document_title: Neurotransmitter

question_text: what is the most abundant neurotransmitter in the nervous system

text: Neurotransmitter

text: Mechanism[edit]

text: Neurotransmitters are stored in a synapse in synaptic vesicles, clustered beneath the membrane in the axon terminal located at the presynaptic side of the synapse. Neurotransmitters are released into and diffused across the synaptic cleft, where they bind to specific receptors in the membrane on the postsynaptic side of the synapse.[3]

text: Most neurotransmitters are about the size of a single amino acid, however, some neurotransmitters may be the size of larger proteins or peptides. A released neurotransmitter is typically available in the synaptic cleft for a short time before it is metabolized by enzymes, pulled back into the presynaptic neuron through reuptake, or bound to a postsynaptic receptor. Nevertheless, short-term exposure of the receptor to a neurotransmitter is typically sufficient for causing a postsynaptic response by way of synaptic transmission.

text: In response to a threshold action potential or graded electrical potential, a neurotransmitter is released at the presynaptic terminal. Low level "baseline" release also occurs without electrical stimulation. The released neurotransmitter may then move across the synapse to be detected by and bind with receptors in the postsynaptic neuron. Binding of neurotransmitters may influence the postsynaptic neuron in either an inhibitory or excitatory way. This neuron may be connected to many more neurons, and if the total of excitatory influences are greater than those of inhibitory influences, the neuron will also "fire". Ultimately it will create a new action potential at its axon hillock to release neurotransmitters and pass on the information to yet another neighboring neuron.[4]

text: Discovery[edit]

text: Until the early 20th century, scientists assumed that the majority of synaptic communication in the brain was electrical. However, through the careful histological examinations by Ramón y Cajal (1852–1934), a 20 to 40 nm gap between neurons, known today as the synaptic cleft, was discovered. The presence of such a gap suggested communication via chemical messengers traversing the synaptic cleft, and in 1921 German pharmacologist Otto Loewi (1873–1961) confirmed that neurons can communicate by releasing chemicals. Through a series of experiments involving the vagus nerves of frogs, Loewi was able to manually slow the heart rate of frogs by controlling the amount of saline solution present around the vagus nerve. Upon completion of this experiment, Loewi asserted that sympathetic regulation of cardiac function can be mediated through changes in chemical concentrations. Furthermore, Otto Loewi is credited with discovering acetylcholine (ACh)—the first known neurotransmitter.[5] Some neurons do, however, communicate via electrical synapses through the use of gap junctions, which allow specific ions to pass directly from one cell to another.[6]

text: Identification[edit]

text: There are four main criteria for identifying neurotransmitters:

text:
The chemical must be synthesized in the neuron or otherwise be present in it.
When the neuron is active, the chemical must be released and produce a response in some target.
The same response must be obtained when the chemical is experimentally placed on the target.
A mechanism must exist for removing the chemical from its site of activation after its work is done.

tag: ol

text: However, given advances in pharmacology, genetics, and chemical neuroanatomy, the term "neurotransmitter" can be applied to chemicals that:

text:
Carry messages between neurons via influence on the postsynaptic membrane.
Have little or no effect on membrane voltage, but have a common carrying function such as changing the structure of the synapse.
Communicate by sending reverse-direction messages that affect the release or reuptake of transmitters.

text: The anatomical localization of neurotransmitters is typically determined using immunocytochemical techniques, which identify the location of either the transmitter substances themselves, or of the enzymes that are involved in their synthesis. Immunocytochemical techniques have also revealed that many transmitters, particularly the neuropeptides, are co-localized, that is, one neuron may release more than one transmitter from its synaptic terminal.[7] Various techniques and experiments such as staining, stimulating, and collecting can be used to identify neurotransmitters throughout the central nervous system.[8]

text: Types[edit]

text: There are many different ways to classify neurotransmitters. Dividing them into amino acids, peptides, and monoamines is sufficient for some classification purposes.

text: Major neurotransmitters:

text:
Amino acids: glutamate,[4] aspartate, D-serine, γ-aminobutyric acid (GABA), glycine
Gasotransmitters: nitric oxide (NO), carbon monoxide (CO), hydrogen sulfide (H2S)
Monoamines: dopamine (DA), norepinephrine (noradrenaline; NE, NA), epinephrine (adrenaline), histamine, serotonin (SER, 5-HT)
Trace amines: phenethylamine, N-methylphenethylamine, tyramine, 3-iodothyronamine, octopamine, tryptamine, etc.
Peptides: somatostatin, substance P, cocaine and amphetamine regulated transcript, opioid peptides[9]
Purines: adenosine triphosphate (ATP), adenosine
Others: acetylcholine (ACh), anandamide, etc.

text: In addition, over 50 neuroactive peptides have been found, and new ones are discovered regularly. Many of these are "co-released" along with a small-molecule transmitter. Nevertheless, in some cases a peptide is the primary transmitter at a synapse. β-endorphin is a relatively well-known example of a peptide neurotransmitter because it engages in highly specific interactions with opioid receptors in the central nervous system.

text: Single ions (such as synaptically released zinc) are also considered neurotransmitters by some,[10] as well as some gaseous molecules such as nitric oxide (NO), carbon monoxide (CO), and hydrogen sulfide (H2S).[11] The gases are produced in the neural cytoplasm and are immediately diffused through the cell membrane into the extracellular fluid and into nearby cells to stimulate production of second messengers. Soluble gas neurotransmitters are difficult to study, as they act rapidly and are immediately broken down, existing for only a few seconds.

text: The most prevalent transmitter is glutamate, which is excitatory at well over 90% of the synapses in the human brain.[4] The next most prevalent is Gamma-Aminobutyric Acid, or GABA, which is inhibitory at more than 90% of the synapses that do not use glutamate. Although other transmitters are used in fewer synapses, they may be very important functionally: the great majority of psychoactive drugs exert their effects by altering the actions of some neurotransmitter systems, often acting through transmitters other than glutamate or GABA. Addictive drugs such as cocaine and amphetamines exert their effects primarily on the dopamine system. The addictive opiate drugs exert their effects primarily as functional analogs of opioid peptides, which, in turn, regulate dopamine levels.

text: List of neurotransmitters, peptides, and gasotransmitters[edit]

text:
Category
Name
Abbreviation
Metabotropic
Ionotropic

Small: Amino acids (Arg)
Arginine

α2-Adrenergic receptors, imidazoline receptors
NMDA receptors

Small: Amino acids
Asparagine
Asp
–
NMDA receptors

Small: Amino acids
Glutamate
Glu
Metabotropic glutamate receptors
NMDA receptors, kainate receptors, AMPARs

Small: Amino acids
Gamma-aminobutyric acid
GABA
GABAB receptors
GABAA receptors, GABAA-ρ receptors

Small: Amino acids
Glycine
Gly
–
NMDA receptors, glycine receptors

Small: Amino acids
D-serine
Ser
–
NMDA receptors

Small: Acetylcholine
Acetylcholine
Ach
Muscarinic acetylcholine receptors
Nicotinic acetylcholine receptors

Small: Monoamine (Phe/Tyr)
Dopamine
DA
Dopamine receptors, trace amine-associated receptor 1[12][13]
–

Small: Monoamine (Phe/Tyr)
Norepinephrine (noradrenaline)
NE, NAd
Adrenergic receptors
–

Small: Monoamine (Phe/Tyr)
Epinephrine (adrenaline)
Epi, Ad
Adrenergic receptors
–

Small: Monoamine (Trp)
Serotonin (5-hydroxytryptamine)
5-HT
Serotonin receptors (all except 5-HT3)
5-HT3

Small: Monoamine (His)
Histamine
H
Histamine receptors
–

Small: Trace amine (Phe)
Phenethylamine
PEA
Human trace amine-associated receptors: hTAAR1, hTAAR2
–

Small: Trace amine (Phe)
N-methylphenethylamine
NMPEA
hTAAR1
–

Small: Trace amine (Phe/Tyr)
Tyramine
TYR
hTAAR1, hTAAR2
–

Small: Trace amine (Phe/Tyr)
Octopamine
Oct
hTAAR1
–

Small: Trace amine (Phe/Tyr)
Synephrine
Syn
hTAAR1
–

Small: Trace amine (Trp)
Tryptamine

hTAAR1, various serotonin receptors
–

Small: Trace amine (Trp)
N-methyltryptamine
NMT
hTAAR1, various serotonin receptors
–

Lipid
Anandamide
AEA
Cannabinoid receptors
–

Lipid
2-Arachidonoylglycerol
2-AG
Cannabinoid receptors
–

Lipid
2-Arachidonyl glyceryl ether
2-AGE
Cannabinoid receptors
–

Lipid
N-Arachidonoyl dopamine
NADA
Cannabinoid receptors
TRPV1

Lipid
Virodhamine

Cannabinoid receptors
–

Small: Purine
Adenosine
Ado
Adenosine receptors
–

Small: Purine
Adenosine triphosphate
ATP
P2Y receptors
P2X receptors

PP: Galanins
Galanin

GALR1, GALR2, GALR3
–

PP: Galanins
Galanin-like peptide

GALR1, GALR2, GALR3
–

PP: Gastrins
Gastrin

Cholecystokinin B receptor
–

PP: Gastrins
Cholecystokinin
CCK
Cholecystokinin receptors
–

PP: Neurohypophyseals
Vasopressin
AVP
Vasopressin receptors
–

PP: Neurohypophyseals
Oxytocin
OT
Oxytocin receptor
–

PP: Neurohypophyseals
Neurophysin I

–
–

PP: Neurohypophyseals
Neurophysin II

–
–

PP: Neuropeptide Y
Neuropeptide Y
NY
Neuropeptide Y receptors
–

PP: Neuropeptide Y
Pancreatic polypeptide
PP
–
–

PP: Neuropeptide Y
Peptide YY
PYY
–
–

PP: Opioids
Enkephalin

δ-Opioid receptor
–

PP: Opioids
Dynorphin

κ-Opioid receptor
–

PP: Opioids
Endorphin

μ-Opioid receptors
–

PP: Opioids
Endomorphin

μ-Opioid receptors
–

PP: Orexins
Orexin A
OX-A
Orexin receptors
–

PP: Orexins
Orexin B
OX-B
Orexin receptors
–

PP: Secretins
Secretin

Secretin receptor
–

PP: Secretins
Motilin

Motilin receptor
–

PP: Secretins
Glucagon

Glucagon receptor
–

PP: Secretins
Vasoactive intestinal peptide
VIP
Vasoactive intestinal peptide receptors
–

PP: Secretins
Growth hormone–releasing hormone
GHRH
Growth hormone–releasing hormone receptor
–

PP: Somatostatins
Somatostatin

Somatostatin receptors
–

PP: Tachykinins
Neurokinin A

–
–

PP: Tachykinins
Neurokinin B

–
–

PP: Tachykinins
Substance P

–
–

PP: Tachykinins
Neuropeptide K

–
–

PP: Other
Adrenocorticotropic hormone
ACTH
ACTH receptor
–

PP: Other
N-Acetylaspartylglutamate
NAAG
Metabotropic glutamate receptor 3 (mGluR3)
–

PP: Other
Cocaine- and amphetamine-regulated transcript
CART
Unknown Gi/Go-coupled receptor[14]
–

PP: Other
Bombesin

–
–

PP: Other
Gastrin releasing peptide
GRP
–
–

PP: Other
Kisspeptin

GPR54
–

Gasotransmitter
Nitric oxide
NO
Soluble guanylyl cyclase
–

Gasotransmitter
Carbon monoxide
CO
–
Heme bound to potassium channels

Gasotransmitter
Hydrogen sulfide
H2S
–
–

text: Actions[edit]

text: Neurons form elaborate networks through which nerve impulses—action potentials—travel. Each neuron has as many as 15,000 connections with neighboring neurons.

text: Neurons do not touch each other (except in the case of an electrical synapse through a gap junction); instead, neurons interact at contact points called synapses: a junction within two nerve cells, consisting of a miniature gap within which impulses are carried by a neurotransmitter. A neuron transports its information by way of a nerve impulse called an action potential. When an action potential arrives at the synapse's presynaptic terminal button, it may stimulate the release of neurotransmitters. These neurotransmitters are released into the synaptic cleft to bind onto the receptors of the postsynaptic membrane and influence another cell, either in an inhibitory or excitatory way. The next neuron may be connected to many more neurons, and if the total of excitatory influences minus inhibitory influences is great enough, it will also "fire". That is to say, it will create a new action potential at its axon hillock, releasing neurotransmitters and passing on the information to yet another neighboring neuron.

text: Excitatory and inhibitory[edit]

text: A neurotransmitter can influence the function of a neuron through a remarkable number of mechanisms. In its direct actions in influencing a neuron’s electrical excitability, however, a neurotransmitter acts in only one of two ways: excitatory or inhibitory. A neurotransmitter influences trans-membrane ion flow either to increase (excitatory) or to decrease (inhibitory) the probability that the cell with which it comes in contact will produce an action potential. Thus, despite the wide variety of synapses, they all convey messages of only these two types, and they are labeled as such. Type I synapses are excitatory in their actions, whereas type II synapses are inhibitory. Each type has a different appearance and is located on different parts of the neurons under its influence. Each neuron receives thousands of excitatory and inhibitory signals every second[citation needed].

text: Type I (excitatory) synapses are typically located on the shafts or the spines of dendrites, whereas type II (inhibitory) synapses are typically located on a cell body. In addition, Type I synapses have round synaptic vesicles, whereas the vesicles of type II synapses are flattened. The material on the presynaptic and post-synaptic membranes is denser in a Type I synapse than it is in a type II, and the type I synaptic cleft is wider. Finally, the active zone on a Type I synapse is larger than that on a Type II synapse.

text: The different locations of type I and type II synapses divide a neuron into two zones: an excitatory dendritic tree and an inhibitory cell body. From an inhibitory perspective, excitation comes in over the dendrites and spreads to the axon hillock to trigger an action potential. If the message is to be stopped, it is best stopped by applying inhibition on the cell body, close to the axon hillock where the action potential originates. Another way to conceptualize excitatory–inhibitory interaction is to picture excitation overcoming inhibition. If the cell body is normally in an inhibited state, the only way to generate an action potential at the axon hillock is to reduce the cell body’s inhibition. In this "open the gates" strategy, the excitatory message is like a racehorse ready to run down the track, but first the inhibitory starting gate must be removed.[15]

text: Examples of important neurotransmitter actions[edit]

text: As explained above, the only direct action of a neurotransmitter is to activate a receptor. Therefore, the effects of a neurotransmitter system depend on the connections of the neurons that use the transmitter, and the chemical properties of the receptors that the transmitter binds to.

text: Here are a few examples of important neurotransmitter actions:

text:
Glutamate is used at the great majority of fast excitatory synapses in the brain and spinal cord. It is also used at most synapses that are "modifiable", i.e. capable of increasing or decreasing in strength. Modifiable synapses are thought to be the main memory-storage elements in the brain. Excessive glutamate release can overstimulate the brain and lead to excitotoxicity causing cell death resulting in seizures or strokes.[16] Excitotoxicity has been implicated in certain chronic diseases including ischemic stroke, epilepsy, amyotrophic lateral sclerosis, Alzheimer's disease, Huntington disease, and Parkinson's disease.[17]
GABA is used at the great majority of fast inhibitory synapses in virtually every part of the brain. Many sedative/tranquilizing drugs act by enhancing the effects of GABA.[18] Correspondingly, glycine is the inhibitory transmitter in the spinal cord.
Acetylcholine was the first neurotransmitter discovered in the peripheral and central nervous systems. It activates skeletal muscles in the somatic nervous system and may either excite or inhibit internal organs in the autonomic system.[8] It is distinguished as the transmitter at the neuromuscular junction connecting motor nerves to muscles. The paralytic arrow-poison curare acts by blocking transmission at these synapses. Acetylcholine also operates in many regions of the brain, but using different types of receptors, including nicotinic and muscarinic receptors.[19]
Dopamine has a number of important functions in the brain; this includes regulation of motor behavior, pleasures related to motivation and also emotional arousal. It plays a critical role in the reward system; Parkinson's disease has been linked to low levels of dopamine and schizophrenia has been linked to high levels of dopamine.[20]
Serotonin is a monoamine neurotransmitter. Most is produced by and found in the intestine (approximately 90%), and the remainder in central nervous system neurons. It functions to regulate appetite, sleep, memory and learning, temperature, mood, behaviour, muscle contraction, and function of the cardiovascular system and endocrine system. It is speculated to have a role in depression, as some depressed patients are seen to have lower concentrations of metabolites of serotonin in their cerebrospinal fluid and brain tissue.[21]
Norepinephrine which focuses on the central nervous system, based on sleep patterns, focus and alertness. It is synthesized from tyrosine.
Epinephrine which is also synthesized from tyrosine takes part in controlling the adrenal glands. It plays a role in sleep, with ones ability to become and stay alert, and the fight-or-flight response.
Histamine works with the central nervous system (CNS), specifically the hypothalamus (tuberomammillary nucleus) and CNS mast cells.

text: Brain neurotransmitter systems[edit]

text: Neurons expressing certain types of neurotransmitters sometimes form distinct systems, where activation of the system affects large volumes of the brain, called volume transmission. Major neurotransmitter systems include the noradrenaline (norepinephrine) system, the dopamine system, the serotonin system, and the cholinergic system, among others. It should be noted that trace amines, primarily via TAAR1 activation, have a very significant effect on neurotransmission in monoamine pathways (i.e., dopamine, histamine, norepinephrine, and serotonin pathways) throughout the brain.[22][23] A brief comparison of these systems follows:

text:
Neurotransmitter systems in the brain

System
Pathway origin and projections
Regulated cognitive processes and behaviors

Noradrenaline system
[24][25][26][27][28][29]
Noradrenergic pathways:

Locus coeruleus (LC) projections

LC → Amygdala and Hippocampus
LC → Brain stem and Spinal cord
LC → Cerebellum
LC → Cerebral cortex
LC → Hypothalamus
LC → Tectum
LC → Thalamus
LC → Ventral tegmental area

Lateral tegmental field (LTF) projections

LTF → Brain stem and Spinal cord
LTF → Olfactory bulb

anxiety
arousal (wakefulness)
circadian rhythm
cognitive control and working memory (co-regulated by dopamine)
feeding and energy homeostasis
medullary control of respiration
negative emotional memory
nociception (perception of pain)
reward (minor role)

Dopamine system
[26][27][28][30][31][32]
Dopaminergic pathways:

Ventral tegmental area (VTA) projections

VTA → Amygdala
VTA → Cingulate cortex
VTA → Hippocampus
VTA → Ventral striatum (Mesolimbic pathway)
VTA → Olfactory bulb
VTA → Prefrontal cortex (Mesocortical pathway)

Nigrostriatal pathway

Substantia nigra pars compacta → Dorsal striatum

Tuberoinfundibular pathway

Arcuate nucleus → Median eminence

arousal (wakefulness)
aversion
cognitive control and working memory (co-regulated by norepinephrine)
emotion and mood
motivation (motivational salience)
motor function
positive reinforcement
reward (primary mediator)
sexual arousal, orgasm, and refractory period (via neuroendocrine regulation)

Histamine system
[27][28][33]
Histaminergic pathways:

Tuberomammillary nucleus (TMN) projections

TMN → Cerebral cortex
TMN → Hippocampus
TMN → Neostriatum
TMN → Nucleus accumbens
TMN → Amygdala
TMN → Hypothalamus

arousal (wakefulness)
feeding and energy homeostasis
learning
memory

Serotonin system
[24][26][27][28][34][35][36]
Serotonergic pathways:
Caudal nuclei (CN):
Raphe magnus, raphe pallidus, and raphe obscurus

Caudal projections

CN → Cerebral cortex
CN → Thalamus
CN → Caudate-putamen and nucleus accumbens
CN → Substantia nigra and ventral tegmental area

Rostral nuclei (RN):
Nucleus linearis, dorsal raphe, medial raphe, and raphe pontis

Rostral projections

RN → Amygdala
RN → Cingulate cortex
RN → Hippocampus
RN → Hypothalamus
RN → Neocortex
RN → Septum
RN → Thalamus
RN → Ventral tegmental area

arousal (wakefulness)
body temperature regulation
emotion and mood, potentially including aggression
feeding and energy homeostasis
reward (minor role)
sensory perception

Acetylcholine system
[24][26][27][28][37]
Cholinergic pathways:
Forebrain cholinergic nuclei (FCN):
Nucleus basalis of Meynert, medial septal nucleus, and diagonal band

Forebrain nuclei projections

FCN → Hippocampus
FCN → Cerebral cortex
FCN → Limbic cortex and sensory cortex

Brainstem cholinergic nuclei (BCN):
Pedunculopontine nucleus, laterodorsal tegmentum, medial habenula, and
parabigeminal nucleus

Brainstem nuclei projections

BCN → Ventral tegmental area
BCN → Thalamus

arousal (wakefulness)
emotion and mood
learning
motor function
motivation (motivational salience)
short-term memory
reward (minor role)

text: Drug effects[edit]

text: Understanding the effects of drugs on neurotransmitters comprises a significant portion of research initiatives in the field of neuroscience. Most neuroscientists involved in this field of research believe that such efforts may further advance our understanding of the circuits responsible for various neurological diseases and disorders, as well as ways to effectively treat and someday possibly prevent or cure such illnesses.[38]

text: Drugs can influence behavior by altering neurotransmitter activity. For instance, drugs can decrease the rate of synthesis of neurotransmitters by affecting the synthetic enzyme(s) for that neurotransmitter. When neurotransmitter syntheses are blocked, the amount of neurotransmitters available for release becomes substantially lower, resulting in a decrease in neurotransmitter activity. Some drugs block or stimulate the release of specific neurotransmitters. Alternatively, drugs can prevent neurotransmitter storage in synaptic vesicles by causing the synaptic vesicle membranes to leak. Drugs that prevent a neurotransmitter from binding to its receptor are called receptor antagonists. For example, drugs used to treat patients with schizophrenia such as haloperidol, chlorpromazine, and clozapine are antagonists at receptors in the brain for dopamine. Other drugs act by binding to a receptor and mimicking the normal neurotransmitter. Such drugs are called receptor agonists. An example of a receptor agonist is Valium, a benzodiazepine that mimics effects of the endogenous neurotransmitter gamma-aminobutyric acid (GABA) to decrease anxiety. Other drugs interfere with the deactivation of a neurotransmitter after it has been released, thereby prolonging the action of a neurotransmitter. This can be accomplished by blocking re-uptake or inhibiting degradative enzymes. Lastly, drugs can also prevent an action potential from occurring, blocking neuronal activity throughout the central and peripheral nervous system. Drugs such as tetrodotoxin that block neural activity are typically lethal.

text: Drugs targeting the neurotransmitter of major systems affect the whole system, which can explain the complexity of action of some drugs. Cocaine, for example, blocks the re-uptake of dopamine back into the presynaptic neuron, leaving the neurotransmitter molecules in the synaptic gap for an extended period of time. Since the dopamine remains in the synapse longer, the neurotransmitter continues to bind to the receptors on the postsynaptic neuron, eliciting a pleasurable emotional response. Physical addiction to cocaine may result from prolonged exposure to excess dopamine in the synapses, which leads to the downregulation of some post-synaptic receptors. After the effects of the drug wear off, an individual can become depressed due to decreased probability of the neurotransmitter binding to a receptor. Fluoxetine is a selective serotonin re-uptake inhibitor (SSRI), which blocks re-uptake of serotonin by the presynaptic cell which increases the amount of serotonin present at the synapse and furthermore allows it to remain there longer, providing potential for the effect of naturally released serotonin.[39] AMPT prevents the conversion of tyrosine to L-DOPA, the precursor to dopamine; reserpine prevents dopamine storage within vesicles; and deprenyl inhibits monoamine oxidase (MAO)-B and thus increases dopamine levels.

text: Agonists[edit]

text: This section needs expansion with: coverage of full agonists and their distinction from partial agonist and inverse agonist.. You can help by adding to it. (August 2015)

text: An agonist is a chemical capable of binding to a receptor, such as a neurotransmitter receptor, and initiating the same reaction typically produced by the binding of the endogenous substance.[40] An agonist of a neurotransmitter will thus initiate the same receptor response as the transmitter. In neurons, an agonist drug may activate neurotransmitter receptors either directly or indirectly. Direct-binding agonists can be further characterized as full agonists, partial agonists, inverse agonists.[citation needed]

text: Direct agonists act similar to a neurotransmitter by binding directly to its associated receptor site(s), which may be located on the presynaptic neuron or postsynaptic neuron, or both.[41] Typically, neurotransmitter receptors are located on the postsynaptic neuron, while neurotransmitter autoreceptors are located on the presynaptic neuron, as is the case for monoamine neurotransmitters;[22] in some cases, a neurotransmitter utilizes retrograde neurotransmission, a type of feedback signaling in neurons where the neurotransmitter is released postsynaptically and binds to target receptors located on the presynaptic neuron.[42][note 1] Nicotine, a compound found in tobacco, is a direct agonist of most nicotinic acetylcholine receptors, mainly located in cholinergic neurons.[43] Opiates, such as morphine, heroin, hydrocodone, oxycodone, codeine, and methadone, are μ-opioid receptor agonists; this action mediates their euphoriant and pain relieving properties.[43]

text: Indirect agonists increase the binding of neurotransmitters at their target receptors by stimulating the release or preventing the reuptake of neurotransmitters.[41] Some indirect agonists trigger neurotransmitter release and prevent neurotransmitter reuptake. Amphetamine, for example, is an indirect agonist of postsynaptic dopamine, norepinephrine, and serotonin receptors in each their respective neurons;[22][23] it produces both neurotransmitter release into the presynaptic neuron and subsequently the synaptic cleft and prevents their reuptake from the synaptic cleft by activating TAAR1, a presynaptic G protein-coupled receptor, and binding to a site on VMAT2, a type of monoamine transporter located on synaptic vesicles within monoamine neurons.[22][23]

text: Antagonists[edit]

text: An antagonist is a chemical that acts within the body to reduce the physiological activity of another chemical substance (as an opiate); especially one that opposes the action on the nervous system of a drug or a substance occurring naturally in the body by combining with and blocking its nervous receptor.[44]

text: There are two main types of antagonist: direct-acting Antagonist and indirect-acting Antagonists:

text:
Direct-acting antagonist- which takes up space present on receptors which are otherwise taken up by neurotransmitters themselves. This results in neurotransmitters being blocked from binding to the receptors. The most common is called Atropine.
Indirect-acting antagonist- drugs that inhibit the release/production of neurotransmitters (e.g., Reserpine).

text: Drug antagonists[edit]

text: An antagonist drug is one that attaches (or binds) to a site called a receptor without activating that receptor to produce a biological response. It is therefore said to have no intrinsic activity. An antagonist may also be called a receptor "blocker" because they block the effect of an agonist at the site. The pharmacological effects of an antagonist therefore result in preventing the corresponding receptor site's agonists (e.g., drugs, hormones, neurotransmitters) from binding to and activating it. Antagonists may be "competitive" or "irreversible".

text: A competitive antagonist competes with an agonist for binding to the receptor. As the concentration of antagonist increases, the binding of the agonist is progressively inhibited, resulting in a decrease in the physiological response. High concentration of an antagonist can completely inhibit the response. This inhibition can be reversed, however, by an increase of the concentration of the agonist, since the agonist and antagonist compete for binding to the receptor. Competitive antagonists, therefore, can be characterized as shifting the dose-response relationship for the agonist to the right. In the presence of a competitive antagonist, it takes an increased concentration of the agonist to produce the same response observed in the absence of the antagonist.

text: An irreversible antagonist binds so strongly to the receptor as to render the receptor unavailable for binding to the agonist. Irreversible antagonists may even form covalent chemical bonds with the receptor. In either case, if the concentration of the irreversible antagonist is high enough, the number of unbound receptors remaining for agonist binding may be so low that even high concentrations of the agonist do not produce the maximum biological response.[45]

text: Precursors[edit]

text:
Biosynthetic pathways for catecholamines and trace amines in the human brain[46][47][48]

L-Phenylalanine
L-Tyrosine
L-DOPA
Epinephrine
Phenethylamine
p-Tyramine
Dopamine
Norepinephrine
N-Methylphenethylamine
N-Methyltyramine
p-Octopamine
Synephrine
3-Methoxytyramine
AADC
AADC
AADC
primary
pathway
PNMT
PNMT
PNMT
PNMT
AAAH
AAAH
brain
CYP2D6
minor
pathway
COMT
DBH
DBH

In humans, catecholamines and phenethylaminergic trace amines are derived from the amino acid L-phenylalanine.

text: While intake of neurotransmitter precursors does increase neurotransmitter synthesis, evidence is mixed as to whether neurotransmitter release and postsynaptic receptor firing is increased. Even with increased neurotransmitter release, it is unclear whether this will result in a long-term increase in neurotransmitter signal strength, since the nervous system can adapt to changes such as increased neurotransmitter synthesis and may therefore maintain constant firing.[49] Some neurotransmitters may have a role in depression and there is some evidence to suggest that intake of precursors of these neurotransmitters may be useful in the treatment of mild and moderate depression.[49][50]

text: Catecholamine and trace amine precursors[edit]

text: L-DOPA, a precursor of dopamine that crosses the blood–brain barrier, is used in the treatment of Parkinson's disease. For depressed patients where low activity of the neurotransmitter norepinephrine is implicated, there is only little evidence for benefit of neurotransmitter precursor administration. L-phenylalanine and L-tyrosine are both precursors for dopamine, norepinephrine, and epinephrine. These conversions require vitamin B6, vitamin C, and S-adenosylmethionine. A few studies suggest potential antidepressant effects of L-phenylalanine and L-tyrosine, but there is much room for further research in this area.[49]

text: Serotonin precursors[edit]

text: Administration of L-tryptophan, a precursor for serotonin, is seen to double the production of serotonin in the brain. It is significantly more effective than a placebo in the treatment of mild and moderate depression.[49] This conversion requires vitamin C.[21] 5-hydroxytryptophan (5-HTP), also a precursor for serotonin, is more effective than a placebo.[49]

text: Diseases and disorders[edit]

text: Diseases and disorders may also affect specific neurotransmitter systems. For example, problems in producing dopamine can result in Parkinson's disease, a disorder that affects a person's ability to move as they want to, resulting in stiffness, tremors or shaking, and other symptoms. Some studies suggest that having too little or too much dopamine or problems using dopamine in the thinking and feeling regions of the brain may play a role in disorders like schizophrenia or attention deficit hyperactivity disorder (ADHD). Similarly, after some research suggested that drugs that block the recycling, or reuptake, of serotonin seemed to help some people diagnosed with depression, it was theorized that people with depression might have lower-than-normal serotonin levels. Though widely popularized, this theory was not borne out in subsequent research.[51] Furthermore, problems with producing or using glutamate have been suggestively and tentatively linked to many mental disorders, including autism, obsessive compulsive disorder (OCD), schizophrenia, and depression.[52]

text: Neurotransmitter imbalance[edit]

text: Generally, there are no scientifically established "norms" for appropriate levels or "balances" of different neurotransmitters. It is in most cases pragmatically impossible to even measure levels of neurotransmitters in a brain or body at any distinct moments in time. Neurotransmitters regulate each other's release, and weak consistent imbalances in this mutual regulation were linked to temperament in healthy people .[53][54][55][56][57] Strong imbalances or disruptions to neurotransmitter systems have been associated with many diseases and mental disorders. These include Parkinson's, depression, insomnia, Attention Deficit Hyperactivity Disorder (ADHD), anxiety, memory loss, dramatic changes in weight and addictions. Chronic physical or emotional stress can be a contributor to neurotransmitter system changes. Genetics also plays a role in neurotransmitter activities. Apart from recreational use, medications that directly and indirectly interact one or more transmitter or its receptor are commonly prescribed for psychiatric and psychological issues. Notably, drugs interacting with serotonin and norepinephrine are prescribed to patients with problems such as depression and anxiety—though the notion that there is much solid medical evidence to support such interventions has been widely criticized.[58]

text: Elimination of neurotransmitters[edit]

text: A neurotransmitter must be broken down once it reaches the post-synaptic cell to prevent further excitatory or inhibitory signal transduction. This allows new signals to be produced from the adjacent nerve cells. When the neurotransmitter has been secreted into the synaptic cleft, it binds to specific receptors on the postsynaptic cell, thereby generating a postsynaptic electrical signal. The transmitter must then be removed rapidly to enable the postsynaptic cell to engage in another cycle of neurotransmitter release, binding, and signal generation. Neurotransmitters are terminated in three different ways:

text:
Diffusion – the neurotransmitter detaches from receptor, drifting out of the synaptic cleft, here it becomes absorbed by glial cells.
Enzyme degradation – special chemicals called enzymes break it down.
Reuptake – re-absorption of a neurotransmitter into the neuron. Transporters, or membrane transport proteins, pump neurotransmitters from the synaptic cleft back into axon terminals (the presynaptic neuron) where they are stored.[59]

text: For example, choline is taken up and recycled by the pre-synaptic neuron to synthesize more ACh. Other neurotransmitters such as dopamine are able to diffuse away from their targeted synaptic junctions and are eliminated from the body via the kidneys, or destroyed in the liver. Each neurotransmitter has very specific degradation pathways at regulatory points, which may be targeted by the body's regulatory system or by recreational drugs.


document_title: Capital punishment in the United Kingdom

question_text: who was the last person to be executed in uk

question_tokens: who was the last person to be executed in uk

root

text: Capital punishment in the United Kingdom

text: Background[edit]

text: Sir Samuel Romilly, speaking to the House of Commons on capital punishment in 1810, declared that "[there is] no country on the face of the earth in which there [have] been so many different offences according to law to be punished with death as in England".[2] Known as the "Bloody Code", at its height the criminal law included some 220 crimes punishable by death, including "being in the company of Gypsies for one month", "strong evidence of malice in a child aged 7–14 years of age" and "blacking the face or using a disguise whilst committing a crime". Many of these offences had been introduced to protect the property of the wealthy classes that emerged during the first half of the 18th century, a notable example being the Black Act of 1723, which created 50 capital offences for various acts of theft and poaching.[citation needed] Crimes eligible for the death penalty included shoplifting and stealing sheep, cattle, and horses, and before abolition of the death penalty for theft in 1832, "English law was notorious for prescribing the death penalty for a vast range of offenses as slight as the theft of goods valued at twelve pence."[3]

tag: p

text: Whilst executions for murder, burglary and robbery were common, the death sentences for minor offenders were often not carried out. A sentence of death could be commuted or respited (permanently postponed) for reasons such as benefit of clergy, official pardons, pregnancy of the offender or performance of military or naval duty.[4] Between 1770 and 1830, an estimated 35,000 death sentences were handed down in England and Wales, of which 7,000 executions were carried out.[5]

text: Reform[edit]

text: This section needs additional citations for verification. Please help improve this article by adding citations to reliable sources. Unsourced material may be challenged and removed. (November 2013) (Learn how and when to remove this template message)

tag: table

text: In 1808 Romilly had the death penalty removed for pickpockets and lesser offenders, starting a process of reform that continued over the next 50 years. The death penalty was mandatory (although it was frequently commuted by the government) until the Judgement of Death Act 1823 gave judges the power to commute the death penalty except for treason and murder. The Punishment of Death, etc. Act 1832 reduced the number of capital crimes by two-thirds. In 1832, the death penalty was abolished for theft, counterfeiting, and forgery except for the forgery of wills and certain powers of attorney.[3][6] Gibbeting was abolished in 1832 and hanging in chains was abolished in 1834. In 1837, the death penalty for forging wills and powers of attorney was abolished. The death penalty for rape was abolished in 1841.[7] In 1861, several acts of Parliament (24 & 25 Vict; c. 94 to c. 100) further reduced the number of civilian capital crimes to five: murder, treason, espionage, arson in royal dockyards, and piracy with violence; there were other offences under military law. The death penalty remained mandatory for treason and murder unless commuted by the monarch.

text: The Royal Commission on Capital Punishment 1864–66[8] concluded (with dissenting Commissioners) that there was not a case for abolition but recommended an end to public executions. This proposal was included in the Capital Punishment Amendment Act 1868. From that date executions in Great Britain were carried out only in prisons. The punishment of beheading and quartering those executed for treason was abolished in 1870.[9] The last application of that punishment had been in 1820 and the last sentence to the punishment had been in 1839.[citation needed]

text: In 1908, the Children Act 1908 banned the execution of juveniles under the age of 16. In 1922 a new offence of Infanticide was introduced to replace the charge of murder for mothers killing their children in the first year of life. In 1930 a parliamentary Select Committee recommended that capital punishment be suspended for a trial period of five years, but no action was taken. From 1931 pregnant women could no longer be hanged (following the birth of their child) although in practice since the 18th century their sentences had always been commuted.

text: In 1933 the minimum age for capital punishment was raised to 18 under the Children and Young Persons Act 1933. The last known execution by the civilian courts of a person under 18 was that of Charles Dobel, 17, hanged at Maidstone together with his accomplice William Gower, 18, in January 1889. Harold Wilkins, at 16 years old, was the last juvenile sentenced to the death penalty in the United Kingdom, in 1932 for a sexually related murder, but he was reprieved due to age.[10]

text: In 1938 the issue of the abolition of capital punishment was brought before parliament. A clause within the Criminal Justice Bill called for an experimental five-year suspension of the death penalty. When war broke out in 1939 the bill was postponed. It was revived after the war and to everyone's surprise was adopted by a majority in the House of Commons (245 to 222). In the House of Lords the abolition clause was defeated but the remainder of the bill was passed. Popular support for abolition was absent and the government decided that it would be inappropriate for it to assert its supremacy by invoking the Parliament Acts 1911 and 1949 over such an unpopular issue.

text: Instead, then Home Secretary, James Chuter Ede, set up a new Royal Commission (the Royal Commission on Capital Punishment, 1949–1953) with instructions to determine "whether the liability to suffer capital punishment should be limited or modified". The Commission's report discussed a number of alternatives to execution by hanging (including the electric chair, gas inhalation, lethal injection, shooting, and the guillotine), but rejected them. It had more difficulty with the principle of capital punishment. Popular opinion believed that the death penalty acted as a deterrent to criminals, but the statistics within the report were inconclusive. Whilst the report recommended abolition from an ethical standpoint, it made no mention of possible miscarriages of justice. The public had by then expressed great dissatisfaction with the verdict in the case of Timothy Evans, who was tried and hanged in 1950 for murdering his infant daughter. It later transpired in 1953 that John Christie had strangled at least six women in the same house; he also confessed to killing Timothy's wife. If the jury in Evans's trial had known this, Evans may have been acquitted. There were other cases in the same period where doubts arose over convictions and subsequent hangings, such as the notorious case of Derek Bentley.

text: The commission concluded that unless there was overwhelming public support in favour of abolition, the death penalty should be retained.

text: Between 1900 and 1949, 621 men and 11 women were executed in England and Wales. Ten German agents were executed during the First World War under the Defence of the Realm Act 1914,[11] and 16 spies were executed during the Second World War under the Treachery Act 1940.[12]

text: By 1957 a number of controversial cases highlighted the issue of capital punishment again. Campaigners for abolition were partially rewarded with the Homicide Act 1957. The Act brought in a distinction between capital and non-capital murder. Only six categories of murder were now punishable by execution:

text:
in the course or furtherance of theft
by shooting or causing an explosion
while resisting arrest or during an escape
of a police officer
of a prison officer by a prisoner
the second of two murders committed on different occasions (if both done in Great Britain).

tag: ul

text: The police and the government were of the opinion that the death penalty deterred offenders from carrying firearms and it was for this reason that such offences remained punishable by death.

text: Abolition[edit]

text: In 1965 the Labour MP Sydney Silverman, who had committed himself to the cause of abolition for more than 20 years, introduced a Private Member's Bill to suspend the death penalty for murder. It was passed on a free vote in the House of Commons by 200 votes to 98. The bill was subsequently passed by the House of Lords by 204 votes to 104.[14][15]

text: The Murder (Abolition of Death Penalty) Act 1965 suspended the death penalty in Great Britain (but not in Northern Ireland) for murder for a period of five years, and substituted a mandatory sentence of life imprisonment; it further provided that if, before the expiry of the five-year suspension, each House of Parliament passed a resolution to make the effect of the Act permanent, then it would become permanent. In 1969 the Home Secretary, James Callaghan, proposed a motion to make the Act permanent, which was carried in the Commons on 16 December 1969,[16] and a similar motion was carried in the Lords on 18 December.[17] The death penalty for murder was abolished in Northern Ireland on 25 July 1973 under the Northern Ireland (Emergency Provisions) Act 1973.

text: Following the abolition of the death penalty for murder, the House of Commons held a vote during each subsequent parliament until 1997 to restore the death penalty. This motion was always defeated, but the death penalty remained for other crimes until the dates mentioned below:

text:
causing a fire or explosion in a naval dockyard, ship, magazine or warehouse (until 1971);
espionage[18] (until 1981);
piracy with violence (until 1998);
treason (until 1998); and
certain purely military offences under the jurisdiction of the armed forces, such as mutiny[19] (until 1998). Prior to its complete abolition in 1998, it was available for six offences:

serious misconduct in action;
assisting the enemy;
obstructing operations;
giving false air signals;
mutiny or incitement to mutiny; and
failure to suppress a mutiny with intent to assist the enemy.

text: However, no executions were carried out in the United Kingdom for any of these offences after the abolition of the death penalty for murder.

text: Nevertheless, there remained a working gallows at HMP Wandsworth, London, until 1994, which was tested every six months until 1992. This gallows is now housed in the Galleries of Justice in Nottingham.[20]

text: Last executions[edit]

text: England and in the United Kingdom: on 13 August 1964, Peter Anthony Allen, at Walton Prison in Liverpool, and Gwynne Owen Evans, at Strangeways Prison in Manchester, were executed for the murder of John Alan West on 7 April that year.[21]

text: Scotland: Henry John Burnett, 21, on 15 August 1963 in Craiginches Prison, Aberdeen, for the murder of seaman Thomas Guyan.

text: Northern Ireland: Robert McGladdery, 26, on 20 December 1961 in Crumlin Road Gaol, Belfast, for the murder of Pearl Gamble.

text: Wales: Vivian Teed, 24, in Swansea on 6 May 1958, for the murder of William Williams, sub-postmaster of Fforestfach Post Office.[22]

text: Last death sentences[edit]

text: Northern Ireland and in the United Kingdom: Liam Holden in 1973 in Northern Ireland, for the capital murder of a British soldier during the Troubles. Holden was removed from the death cell in May 1973.[23] In 2012 his conviction was quashed on appeal.[24]

text: England: David Chapman, who was sentenced to hang in November 1965 for the murder of a swimming pool nightwatchman in Scarborough. He was released from prison in 1979 and later died in a car accident.

text: Scotland: Patrick McCarron in 1964 for shooting his wife. He committed suicide in prison in 1970.

text: Wales: Edgar Black, who was reprieved on 6 November 1963. He had shot his wife's lover in Cardiff.

text: Final abolition[edit]

text: The Criminal Damage Act 1971 abolished the offence of arson in royal dockyards.

text: The Naval Discipline Act 1957 reduced the scope of capital espionage from "all spies for the enemy" to spies on naval ships or bases.[25] Later, the Armed Forces Act 1981 abolished the death penalty for espionage.[26] (The Official Secrets Act 1911 had created another offence of espionage which carried a maximum sentence of fourteen years.)

text: Beheading was abolished as a method of execution for treason in 1973.[27] Hanging, however, remained available until 1998 when, under a House of Lords amendment to the Crime and Disorder Act 1998, proposed by Lord Archer of Sandwell, the death penalty was abolished for treason and piracy with violence, replacing it with a discretionary maximum sentence of life imprisonment. These were the last civilian offences punishable by death.

text: On 20 May 1998 the House of Commons voted to ratify the 6th Protocol of the European Convention on Human Rights prohibiting capital punishment except "in time of war or imminent threat of war". The last remaining provisions for the death penalty under military jurisdiction (including in wartime) were removed when section 21(5) of the Human Rights Act 1998 came into force on 9 November 1998. On 10 October 2003, effective from 1 February 2004,[28] the UK acceded to the 13th Protocol, which prohibits the death penalty in all circumstances.[29]

text: As a legacy from colonial times, several states in the West Indies still had the British Judicial Committee of the Privy Council as the court of final appeal; although the death penalty has been retained in these states, the Privy Council would sometimes delay or deny executions. Some of these states severed links with the British court system in 2001 by transferring the responsibilities of the Privy Council to the Caribbean Court of Justice, to speed up executions.[30]

text: Crown dependencies[edit]

text: Although not part of the United Kingdom, the Isle of Man and the bailiwicks of Guernsey and Jersey are British Crown dependencies.

text: In the Channel Islands, the last death sentence was passed in 1984; the last execution in the Channel Islands was in Jersey on 9 October 1959, when Francis Joseph Huchet was hanged for murder.[31] The Human Rights (Amendment) (Jersey) Order 2006[32] amends the Human Rights (Jersey) Law 2000[33] to give effect to the 13th Protocol of the European Convention on Human Rights providing for the total abolition of the death penalty. Both of these laws came into effect on 10 December 2006. Capital punishment was abolished in Guernsey in 2003, and the 13th Protocol was extended to Guernsey in April 2004. Sark formally retained it until January 2004, when the Chief Pleas in a 14–9 vote removed it from the statutes.[34][35]

text: The last execution on the Isle of Man took place in 1872, when John Kewish was hanged for patricide. Capital punishment was not formally abolished by Tynwald (the island's parliament) until 1993.[36] Five persons were sentenced to death (for murder) on the Isle of Man between 1973 and 1992, although all sentences were commuted to life imprisonment. The last person to be sentenced to death in the UK or its dependencies was Anthony Teare, who was convicted at the Manx Court of General Gaol Delivery in Douglas for contract murder in 1992; he was subsequently retried and sentenced to life imprisonment in 1994.[37] In 2004 the 13th Protocol was adopted,[38] with an effective date of 1 November 2006.[39]

text: Overseas territories[edit]

text: Like the Crown dependencies, the British overseas territories are constitutionally not part of the United Kingdom. However, the British government's ultimate responsibility for good governance of the territories has led it over recent years to pursue a policy of revoking all statutory provision for the death penalty in those territories where it had up until recently been legal.

text: The last executions in an overseas territory, and indeed the last on British soil, took place in Bermuda in 1977, when two men, Larry Tacklyn and Erskine Burrows, were hanged for the 1973 murder of the territory's then Governor Sir Richard Sharples.[40]

text: In 1991, the British government extended an Order in Council to its Caribbean territories whose effect was to abolish capital punishment for murder: Anguilla, the British Virgin Islands, the Cayman Islands, Montserrat and the Turks and Caicos Islands.[41]

text: The British government was unable to extend the abolition via Order in Council to Bermuda, the UK's most autonomous overseas territory with powers of almost total self-governance—but warned that if voluntary abolition was not forthcoming it would be forced to consider the unprecedented step of "whether to impose abolition by means of an Act of Parliament".[42] As a result, the Bermudian government introduced its own domestic legislation in 1999 to rectify the problem.[43]

text: Further measures were subsequently adopted to revoke technicalities in British overseas territories' domestic legislation as regards use of the death penalty for crimes of treason and piracy. In October 2002 the British government abolished the death penalty for treason and piracy in the Turks and Caicos Islands. Since then, the death penalty has been outlawed under all circumstances in all the UK's overseas territories.[44]

text: Public support for reintroduction of capital punishment[edit]

text: Since the death penalty's suspension in 1965, there have been continued public and media calls for its reintroduction, particularly prompted by high-profile murder cases.

text: At the same time, there have been a number of miscarriages of justice since 1965 where someone convicted of murder has later had their conviction quashed on appeal and been released from prison, strengthening the argument of those who oppose the death penalty's reintroduction. These include the Birmingham Six (cleared in 1991 of planting an IRA bomb which killed 21 people in 1974), the Guildford Four (cleared in 1989 of murdering five people in another 1974 IRA bombing), Stephen Downing (a Derbyshire man who was freed in 2001 after serving 27 years for the murder of a woman in a churchyard) and Barry George (who was freed in 2007 when his conviction for the 1999 murder of TV presenter Jill Dando was quashed on appeal).[45]

text: Perhaps the first high-profile murder case which sparked widespread calls for a return of the death penalty was the Moors murders trial in 1966, the year after the death penalty's suspension, in which Ian Brady and Myra Hindley were sentenced to life imprisonment for the murders of two children and a teenager in the Manchester area (they later confessed to a further two murders).[46] Later in 1966, the murder of three policemen in West London also attracted widespread public support for the death penalty's return.[47] Other subsequent high-profile cases to have sparked widespread media and public calls for the death penalty's return include "Yorkshire Ripper" Peter Sutcliffe, convicted in 1981 of murdering 13 women and attacking seven others in the north of England,[48] Roy Whiting, who murdered a seven-year-old girl in West Sussex in 2000,[49] and Ian Huntley, a Cambridgeshire school caretaker who killed two 10-year-old girls in 2002.[50]

text: A November 2009 television survey showed that 70% favoured reinstating the death penalty for at least one of the following crimes: armed robbery, rape, crimes related to paedophilia, terrorism, adult murder, child murder, child rape, treason, child abuse or kidnapping. However, respondents only favoured capital punishment for adult murder, the polling question asked by other organisations such as Gallup, by small majorities or pluralities: overall, 51% favoured the death penalty for adult murder, while 56% in Wales did, 55% in Scotland, and only 49% in England.[51]

text: In August 2011, the Internet blogger Paul Staines—who writes a political blog as Guido Fawkes and heads the Restore Justice Campaign—launched an e-petition on the Downing Street website calling for the restoration of the death penalty for those convicted of the murder of children and police officers.[52] The petition was one of several in support or opposition of capital punishment to be published by the government with the launch of its e-petitions website. Petitions attracting 100,000 signatures would prompt a parliamentary debate on a particular topic, but not necessarily lead to any Parliamentary Bills being put forward.[53] When the petition closed on 4 February 2012 it had received 26,351 signatures in support of restoring capital punishment,[54] but a counter-petition calling to retain the ban on capital punishment received 33,455 signatures during the same time period.[55]

text: Also in August 2011, a representative survey conducted by Angus Reid Public Opinion showed that 65% of Britons support reinstating the death penalty for murder in Great Britain, while 28% oppose this course of action. Men and respondents aged over 35 are more likely to endorse the change.[56]

text: In March 2015 a survey by the NatCen British Social Attitudes Report showed that public support for the death penalty had dropped to 48 per cent.[57]

text: Parliamentary debates on reintroduction[edit]

text: After Royal Assent for the Murder (Abolition of Death Penalty) Act 1965, supporters in Parliament have made several attempts to reintroduce capital punishment. On 23 November 1966, Duncan Sandys was refused leave to bring in a Bill to restore capital punishment for the murder of police or prison officers, by a vote of 170 to 292.[58] Motions to make the five-year suspension of capital punishment under the 1965 Act permanent were opposed, but agreed by 343 to 185 in the House of Commons;[59] in the House of Lords, an amendment to continue with a temporary suspension of capital punishment until 31 July 1973 was rejected by 174 to 220.[60] In April 1973, the House of Commons voted against reintroduction.[61]

text: The deaths of civilians in several IRA bombings in 1974 prompted a renewed debate. On 11 December 1974 Brian Walden moved a motion declaring that "the death penalty would neither deter terrorists nor increase the safety of the public"; Jill Knight moved an amendment calling instead for introduction of legislation providing for death to be the penalty for acts of terrorism causing death. Her amendment was rejected by 217 to 369.[62] A year later, Ivan Lawrence's motion "That this House demands capital punishment for terrorist offences causing death" was rejected by 232 to 361.[63]

text: After the Conservatives' victory in the 1979 general election, Eldon Griffiths (Parliamentary adviser to the Police Federation of England and Wales) moved a motion "that the sentence of capital punishment should again be available to the courts" on 19 July 1979.[64] While the motion was not expected to pass, the margin of its defeat (243 to 362) was much wider than expected.[65] Later in the same Parliament, the Criminal Justice Bill provided an opportunity on 11 May 1982 for several new clauses to be proposed which would have reinstated capital punishment. The first, which simply declared that "A person convicted of murder shall be liable to capital punishment", was tabled by Edward Gardner, and rejected by 195 to 357.[66] It was followed by an alternative under which capital punishment would be available "as the penalty for an act of terrorism involving the loss of human life"; this new clause was rejected by 176 to 332.[67] A further new clause proposing capital punishment "as the penalty for murder by means of firearms or explosives" was rejected by 176 to 343.[68] Then a new clause allowing for capital punishment "as the penalty for murder of a police or prison officer" was rejected by 208 to 332.[69] Finally a new clause allowing capital punishment "as the penalty for murder in the course of robbery and burglary which involves the use of offensive weapons" was rejected by 151 to 331.[70]

text: The new Parliament in 1983 again prompted supporters of capital punishment to put their case. Sir Edward Gardner's motion "That this House favours the restoration of the death penalty for murder" was debated on 13 July 1983, with several amendments moved to restrict capital punishment to certain categories of murder. The amendments were voted on first: capital punishment for murder "resulting from acts of terrorism" was rejected by 245 to 361, for murder "of a police officer during the course of his duties" by 263 to 344, for murder "of a prison officer during the course of his duties" by 252 to 348, for murder "by shooting or causing an explosion" by 204 to 374, and for murder "in the course or furtherance of theft" by 194 to 369. The main motion was then defeated by 223 to 368.[71] Towards the end of the Parliament, a new clause proposed to the Criminal Justice Bill proposed to return the death penalty for "A person convicted by the unanimous verdict of a jury of the premeditated killing of another person or of knowingly and intentionally killing another person in a manner, or for a reason, or in circumstances which a reasonable person would consider to be evil" was rejected by 230 to 342 on 1 April 1987.[72]

text: The Criminal Justice Bill in 1988 provided a further opportunity for a debate; the new clause proposed by Roger Gale allowed for the jury in a murder case to "have the power, upon reaching a verdict of guilt of murder, to recommend .. death in the manner authorised by law". It was rejected by 218 to 341.[73]

text: The aforementioned bills were rejected despite support from then Prime Minister Margaret Thatcher.[74]

text: On 17 December 1990 a new Criminal Justice Bill again saw amendments designed to reintroduce capital punishment. The first covered anyone over 18 "convicted of the murder of a police officer acting in the execution of his duty" and was rejected by 215 to 350;[75] a general reintroduction of death as the penalty for murder (with special provision for the Court of Appeal to decide whether to substitute a life sentence) was then rejected by 182 to 367.[76] Capital punishment for "murder committed by means of firearms, explosives or an offensive weapon, or for the murder of a police or prison officer" was rejected by 186 to 349.[77]

text: The most recent Parliamentary debate on a question proposing reintroduction of capital punishment came on 21 February 1994 when new clauses to the Criminal Justice and Public Order Bill were moved. The first, providing for death as the sentence for "the murder of a police officer acting in the execution of his duty", was rejected by 186 to 383;[78] A new clause providing for general reintroduction with power for the Court of Appeal to substitute life imprisonment was rejected by 159 to 403.[79] This would have been aimed at terrorists in the Northern Ireland conflict.[80]

text: In June 2013 a new bill for capital punishment in England and Wales was introduced. This Bill has been withdrawn and will not progress any further.[81]

text: Parties' stance on the issue[edit]

text: This section does not cite any sources. Please help improve this section by adding citations to reliable sources. Unsourced material may be challenged and removed. (August 2017) (Learn how and when to remove this template message)

text: The following parties support the reintroduction of capital punishment:

text:
National Front (NF)
British National Party (BNP)
British Democratic Party
Britain First

text: Notable executions in the United Kingdom[edit]

text: Before 1707[edit]

text:
13 April 1546: Alice Glaston, the youngest known girl legally executed in England, at age 11 for an unknown offence.[82][83][84][85][86][87]
23 February 1629: John Dean, the youngest known person legally executed in England, at age 8 or 9 for arson.[84][88]

text: Kingdom of Great Britain, 1707–1801[edit]

text:
16 November 1724: Jack Sheppard, housebreaker, was hanged at Tyburn for burglary after four successful escape attempts from jail. His partner-in-crime, highwayman Joseph "Blueskin" Blake, was executed for the same burglary five days earlier.
24 May 1725: Jonathan Wild, criminal overlord and fraudulent "Thief Taker General", was hanged at Tyburn for receiving stolen goods and thus aiding criminals.
7 April 1739: Dick Turpin, famous highwayman, was hanged.
30 July 1746: nine Catholic members of the Manchester Regiment, Jacobites, were hanged, drawn and quartered for treason at Kennington Common (now Kennington Park).
9 April 1747: Simon Fraser, 11th Lord Lovat, Jacobite leader and Scottish Clan chief, at Tower Hill, the last man to be publicly beheaded in Britain.
3 October 1750: James MacLaine, 'The Gentleman Highwayman', was hanged at Tyburn, London
14 March 1757: John Byng became the only British admiral executed, by firing squad by the Royal Navy. His crime was having failed to "do his utmost" at the Battle of Minorca during the Seven Years' War.
5 May 1760: Laurence Shirley, 4th Earl Ferrers was executed at Tyburn for the murder of a servant.[89] He was the last peer to be hanged (reputedly by a silken rope) and is the only peer to have been hanged for murder.
18 March 1789: Catherine Murphy, a counterfeiter, was the last woman in England to be burned at the stake (though she was in fact strangled before the fire was lit, and thus not literally burned to death). The penalty of burning at the stake, which at the time applied to women and not to men, was abolished the next year.[90]

text: United Kingdom of Great Britain and Ireland, 1801–1922[edit]

text:
13 November 1805: Richard Harding was hanged for knowingly uttering playing cards with forged ace of spades.
18 May 1812: John Bellingham was hanged for the murder of Prime Minister Spencer Perceval.
8 September 1820: Andrew Hardie and John Baird were hanged and beheaded at Stirling after being tried for their part in the Radical War in Scotland.
11 August 1828: William Corder was hanged at Bury St Edmunds for the murder of Maria Marten at the Red Barn a year before.
9 August 1856: Elizabeth Martha Brown was the last woman to be hanged in public in the English county of Dorset; her hanging is notable in part because it influenced Thomas Hardy, an eyewitness, in his portrayal of the execution of the fictional heroine of Tess of the D'Urbervilles.
27 August 1861: Martin Doyle was the last person to be hanged for attempted murder, at Chester.
14 November 1864: Franz Muller was hanged for the murder of Thomas Briggs, the first murder committed on a British train.
2 April 1868: Frances Kidder was the last woman to be hanged in public in Britain.[91]
26 May 1868: Fenian Michael Barrett was executed at Newgate Prison for mass murder. He had participated in the Clerkenwell explosion, which had killed 12 people. His execution was the last public hanging in the UK.
19 July 1899: Mary Ansell was hanged at St Albans, for poisoning her sister. At 22, she was the youngest woman to be hanged in the post-1868 'modern era' (non-public, and by the 'long drop' method).
23 November 1910: Hawley Harvey Crippen was hanged in London's Pentonville Prison for poisoning his wife.
8 September 1914: Private Thomas Highgate was executed by firing squad, the first British soldier to be executed for desertion during World War I.
13 August 1915: George Joseph Smith was hanged in Maidstone Prison for the pattern of serial killings known as the "Brides in the Bath Murders".
3 August 1916: Roger Casement was hanged at Pentonville for treason, he was convicted of conspiring with Germany, then at war with the United Kingdom, to incite insurrection in Ireland and to incite Irish soldiers serving in the British Army to mutiny.

text: United Kingdom of Great Britain and Northern Ireland, 1922–1964[edit]

text:
9 January 1923: Edith Thompson and Frederick Bywaters, in London's Holloway and Pentonville Prisons respectively, for the murder of Thompson's husband. The case was controversial because, although in letters Thompson had fantasised about the possible elimination of her husband, there was no firm evidence that she was in any way connected with the murder for which she was hanged.
3 January 1931: Victor Betts for murder committed during the course of a robbery. The case had established that a person need not be present when a crime is committed to be regarded as an accessory after the fact.[92]
31 July 1940: Udham Singh, an Indian independence activist, at Pentonville Prison. He had assassinated the Indian administrator Sir Michael O'Dwyer.
15 August 1941: Josef Jakobs, a German spy, was executed by firing squad, the last execution in the Tower of London.
19 December 1945; John Amery, a British fascist and Nazi collaborator, pleaded guilty of eight charges of treason. Hanged at Wandsworth Prison in London.
3 January 1946: William Joyce, better known as "Lord Haw-Haw", for treason in London's Wandsworth Prison. He was an American citizen, but was convicted of treason because, as the holder of a British passport (albeit fraudulently obtained), he was held to have owed allegiance to the British sovereign. Theodore Schurch, hanged for treachery the next day, was the last person to be executed for an offence other than murder; he was executed at Pentonville. As a member of the armed forces he had been tried by court-martial.
27 February 1947: Walter Rowland in Manchester for the murder of Olive Balchin despite maintaining his innocence. While he had been awaiting execution, another man confessed to the crime. A Home Office report dismissed the latter's confession as a fake, but in 1951 he attacked another woman and was found guilty but insane.[93]
12 January 1949: Margaret Allen, aged 43, for killing a 70-year-old woman in the course of a robbery, the first woman to be hanged in Britain for 12 years.
10 August 1949: John George Haigh, the "acid-bath murderer", at Wandsworth.
9 March 1950: Timothy Evans at Pentonville for the murder of his baby daughter Geraldine at 10 Rillington Place, North West London. He initially claimed to have killed his wife, but later withdrew the claim. A fellow inhabitant at the same address, John Christie, later found to be a sexual serial killer, gave key evidence against Evans. Christie was executed in 1953 for the murder of his own wife. Evans received a posthumous pardon in 1966. In 2004 the Court of Appeal refused to consider overturning the conviction due to the costs and resources that would be involved. See John Christie (murderer).
28 March 1950: George Kelly at Liverpool for murder, but had his conviction quashed posthumously by the Court of Appeal in June 2003.
25 April 1952: Edward Devlin and Alfred Burns, for killing a woman during a robbery in Liverpool. They claimed that they had been doing a different burglary in Manchester, and others involved in the crime supported this. A Home Office report rejected this evidence. Huge crowds gathered outside Liverpool's Walton Prison as they were executed.
3 September 1952: Mahmood Hussein Mattan, a Somali seaman, in Cardiff for murder. The Court of Appeal quashed his conviction posthumously in 1998[94] after hearing that crucial evidence implicating another Somali was withheld at his trial.
28 January 1953: Derek Bentley at Wandsworth Prison as an accomplice to the murder of a police officer by his 16-year-old friend Christopher Craig. Craig, a minor, was not executed and instead served 10 years. Bentley was granted a partial posthumous pardon on 29 July 1993, and the Court of Appeal fully overturned his conviction on 30 July 1998.
15 July 1953: John Christie at Pentonville for the murder of his wife Ethel. Christie was a serial killer and had murdered at least six other women (see also entry on Timothy Evans above).
13 December 1954: Styllou Christofi, aged 53, penultimate woman executed in Britain.
13 July 1955: Ruth Ellis, aged 28, the last woman to be hanged in Britain. She was the 15th and youngest woman hanged in the 20th century.
6 May 1958: Vivian Teed, 24, in Swansea, the last person to be executed in Wales.
11 July 1958: Peter Manuel, aged 31, second to last person to be hanged in HM Prison Barlinnie and the third to last to be hanged in Scotland.
5 November 1959: Guenther Podola, the last person to be hanged for the murder of a policeman.
10 November 1960: Francis Forsyth, the last 18-year-old to be executed in Britain.
22 December 1960: Anthony Miller, 19, in Glasgow's Barlinnie Prison, the last teenager to be executed in Britain.
20 December 1961: Robert McGladdery, 25, in Crumlin Road Gaol in Belfast, the last person to be executed in Northern Ireland, for the murder of Pearl Gamble in Newry.
4 April 1962: James Hanratty at Bedford after a controversial rape-murder trial. In 2002 Hanratty's body was exhumed and the Court of Appeal upheld his conviction after Hanratty's DNA was linked to crime scene samples.
15 August 1963: Henry Burnett, aged 21, at Craiginches Prison in Aberdeen for the murder of seaman Thomas Guyan, the last hanging in Scotland.
13 August 1964: Peter Anthony Allen, at Walton Prison in Liverpool, and Gwynne Owen Evans, at Strangeways Prison in Manchester for the murder of John Alan West, the last people executed in Britain.[21][95]