Neurotransmitter

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For an introduction to concepts and terminology used in this article, see Chemical synapse.
Structure of a typical chemical synapse

Neurotransmitters are endogenous chemicals that enable neurotransmission. They transmit signals across a chemical synapse, such as in a neuromuscular junction, from one neuron (nerve cell) to another "target" neuron, muscle cell, or gland cell.[1] Neurotransmitters are released from synaptic vesicles in synapses into the synaptic cleft, where they are received by receptors on other synapses. Many neurotransmitters are synthesized from simple and plentiful precursors such as amino acids, which are readily available from the diet and only require a small number of biosynthetic steps to convert them. Neurotransmitters play a major role in shaping everyday life and functions. Their exact numbers are unknown but more than 100 chemical messengers have been identified.[2]

Mechanism

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]

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.

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]

Discovery

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]

Identification

There are four main criteria for identifying neurotransmitters:

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

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

  • 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 have an impact on the release or reuptake of transmitters.

The anatomical localization of neurotransmitters is typically determined using immunocytochemical techniques, which identify either 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]

Types

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

Major neurotransmitters:

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.

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.

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.

List of neurotransmitters, peptides, and gasotransmitters

Category Name Abbreviation Metabotropic Ionotropic
Small: Amino acids (Arg) Agmatine α2 adrenergic receptor Imidazoline receptor NMDA receptor
Small: Amino acids Aspartate Asp – NMDA receptor
Small: Amino acids Glutamate (glutamic acid) Glu Metabotropic glutamate receptor NMDA receptor (co-agonist), Kainate receptor, AMPA receptor
Small: Amino acids Gamma-aminobutyric acid GABA GABAB receptor GABAA, GABAA-ρ receptor
Small: Amino acids Glycine Gly – Glycine receptor, NMDA receptor (co-agonist)
Small: Amino acids D-serine Ser – NMDA receptor (co-agonist)
Small: Acetylcholine Acetylcholine Ach Muscarinic acetylcholine receptor Nicotinic acetylcholine receptor
Small: Monoamine (Phe/Tyr) Dopamine DA Dopamine receptor –
Small: Monoamine (Phe/Tyr) Norepinephrine (noradrenaline) NE, NAd Adrenergic receptor –
Small: Monoamine (Phe/Tyr) Epinephrine (adrenaline) Epi, Ad Adrenergic receptor –
Small: Monoamine (Trp) Serotonin (5-hydroxytryptamine) 5-HT Serotonin receptor, all but 5-HT3 5-HT3
Small: Monoamine (Trp) Melatonin Mel Melatonin receptor –
Small: Monoamine (His) Histamine H Histamine receptor –
Small: Trace amine (Phe) Phenethylamine PEA 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 (Phe/Tyr) 3-methoxytyramine 3-MT hTAAR1 –
Small: Trace amine (Trp) Tryptamine hTAAR1, various 5-HT receptors
Small: Trace amine (Trp) N-methyltryptamine NMT hTAAR1, various 5-HT receptors,
Neuropeptides N-Acetylaspartylglutamate NAAG Metabotropic glutamate receptors; selective agonist of mGluR3 –
PP: Gastrins Gastrin – –
PP: Gastrins Cholecystokinin CCK Cholecystokinin receptor –
PP: Neurohypophyseals Vasopressin AVP Vasopressin receptor –
PP: Neurohypophyseals Oxytocin OT Oxytocin receptor –
PP: Neurohypophyseals Neurophysin I – –
PP: Neurohypophyseals Neurophysin II – –
PP: Neuropeptide Y Neuropeptide Y NY Neuropeptide Y receptor –
PP: Neuropeptide Y Pancreatic polypeptide PP – –
PP: Neuropeptide Y Peptide YY PYY – –
PP: Opioids Corticotropin (adrenocorticotropic hormone) ACTH Corticotropin receptor –
PP: Opioids Enkephaline δ-opioid receptor –
PP: Opioids Dynorphin κ-opioid receptor –
PP: Opioids Endorphin μ-opioid receptor –
PP: Orexins Orexin A OX-A Orexin receptor –
PP: Orexins Orexin B OX-B Orexin receptor –
PP: Secretins Secretin Secretin receptor –
PP: Secretins Motilin Motilin receptor –
PP: Secretins Glucagon Glucagon receptor –
PP: Secretins Vasoactive intestinal peptide VIP Vasoactive intestinal peptide receptor –
PP: Secretins Growth hormone-releasing factor GRF – –
PP: Somatostatins Somatostatin Somatostatin receptor –
SS: Tachykinins Neurokinin A – –
SS: Tachykinins Neurokinin B – –
SS: Tachykinins Substance P – –
PP: Other Cocaine and amphetamine regulated transcript CART Unknown Gi/Go-coupled receptor[12]
PP: Other Bombesin – –
PP: Other Gastrin releasing peptide GRP – –
Gas Nitric oxide NO Soluble guanylyl cyclase –
Gas Carbon monoxide CO – Heme bound to potassium channels
Small: Endocannabinoid Anandamide AEA Cannabinoid receptor –
Small: Endocannabinoid 2-Arachidonoylglycerol 2-AG Cannabinoid receptor –
Small: Endocannabinoid 2-Arachidonyl glyceryl ether 2-AGE Cannabinoid receptor –
Small: Endocannabinoid N-Arachidonoyl dopamine NADA Cannabinoid receptor TRPV1
Small: Endocannabinoid Virodhamine Cannabinoid receptor –
Purine Adenosine triphosphate ATP P2Y P2X
Purine Adenosine Ado Adenosine receptor –

Actions

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

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 which impulses pass 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 is greater than that of inhibitory influences, 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.

Excitatory and inhibitory

File:The synthesis, packaging, secretion, and removal of neurotransmitters..jpg
The synthesis, packaging, secretion, and removal of neurotransmitters.

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.

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.

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.[13]

Examples of important neurotransmitter actions

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.

Here are a few examples of important neurotransmitter actions:

Brain neurotransmitter systems

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 impact on neurotransmission in monoamine pathways (i.e., dopamine, histamine, norepinephrine, and serotonin pathways) throughout the brain.[20][21] A brief comparison of these systems follows:

Neurotransmitter systems in the brain
System Pathway origin and projections Regulated psychological processes and behaviors
Noradrenaline system
[22][23][24]		 Noradrenergic pathways:
Dopamine system
[24][25]		 Dopaminergic pathways:
Histamine system
[26]		 Histaminergic pathways:
Serotonin system
[22][24][27][28]		 Serotonergic pathways:

Caudal nuclei (CN):
Raphe magnus, raphe pallidus, and raphe obscuris

  • Caudal projections

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

  • Rostral projections
Acetylcholine system
[22][24][29]		 Cholinergic pathways:

Forebrain cholinergic nuclei (FCN):
Nucleus basalis of Meynert, medial septal nucleus, and diagonal band

  • Forebrain nuclei projections

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

  • Brainstem nuclei projections

Drug effects

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.[30]

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.

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.[31] 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.

Agonists

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Main article: Agonist

Lua error in package.lua at line 80: module 'strict' not found. 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.[32] 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]

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.[33] 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;[20] 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.[34][note 1] Nicotine, a compound found in tobacco, is a direct agonist of most nicotinic acetylcholine receptors, mainly located in cholinergic neurons.[35] Opiates, such as morphine, heroin, hydrocodone, oxycodone, codeine, and methadone, are μ-opioid receptor agonists; this action mediates their euphoriant and pain relieving properties.[35]

Indirect agonists increase the binding of neurotransmitters at their target receptors by stimulating the release or preventing the reuptake of neurotransmitters.[33] 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;[20][21] 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.[20][21]

Antagonists

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Main article: Receptor antagonist

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.[36]

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

  1. 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.
  2. Indirect-acting antagonist- drugs that inhibit the release/production of neurotransmitters (e.g., Reserpine).

Drug antagonists

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".

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.

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.[37]

Precursors

Human biosynthesis pathway for trace amines and catecholamines[38][39]
The image above contains clickable links
In humans, catecholamines and phenethylaminergic trace amines are derived from the amino acid phenylalanine.

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.[40] 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.[40][41]

Catecholamine and trace amine precursors

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.[40]

Serotonin precursors

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.[40] This conversion requires vitamin C.[19] 5-hydroxytryptophan (5-HTP), also a precursor for serotonin, is more effective than a placebo.[40]

Diseases and disorders

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 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). Moreover, research shows that people diagnosed with depression often have lower than normal levels of serotonin. The types of medications most commonly prescribed to treat depression act by blocking the recycling, or reuptake, of serotonin by the sending neuron. As a result, more serotonin stays in the synapse for the receiving neuron to bind onto, leading to more normal mood functioning. Furthermore, problems in making or using glutamate have been linked to many mental disorders, including autism, obsessive compulsive disorder (OCD), schizophrenia, and depression.[42]

CAPON Binds Nitric Oxide Synthase, Regulating NMDA Receptor–Mediated Glutamate Neurotransmission

Elimination of neurotransmitters

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:

  1. Diffusion – the neurotransmitter detaches from receptor, drifting out of the synaptic cleft, here it becomes absorbed by glial cells.
  2. Enzyme degradation – special chemicals called enzymes break it down.
  3. 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.[43]

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.

Neurotransmitter imbalance

Neurotransmitter imbalances have been connected to the cause of many diseases. These include Parkinson's, depression, insomnia, Attention Deficit Hyperactivity Disorder (ADHD), anxiety, memory loss, dramatic changes in weight and addictions. They all involve amino acids which form neurotransmitters. The acids are made up of protein and without a sufficient amount of this then cells are not structured properly; therefore not functioning properly. Chronic stress is the primary contributor to neurotransmitter imbalance. Physical and emotional stress from a job or a relationship causes neurons to use up large amounts of neurotransmitters in order to cope with the ongoing stress. Over time the stress wears out the nervous system and depletes neurotransmitter supply. Genetics play a part in correlating with neurotransmitter imbalance. Some people are already born with neurotransmitter deficiencies or excesses. Scientists are trying to supplement medication by changing the diets of some patients instead; adding amino acids into the body. Medications that directly react with serotonin and norepinephrine are prescribed to patients with diseases such as depression and anxiety disorders.[44]

See also

Notes

  1. ↑ In the central nervous system, anandamide other endocannabinoids utilize retrograde neurotransmission, since their release is postsynaptic, while their target receptor, cannabinoid receptor 1 (CB1), is presynaptic.[34] The cannabis plant contains Δ9-tetrahydrocannabinol, which is a direct agonist at CB1.[34]

References

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  4. ↑ 4.0 4.1 4.2 Lua error in package.lua at line 80: module 'strict' not found.
  5. ↑ Saladin, Kenneth S. Anatomy and Physiology: The Unity of Form and Function. McGraw Hill. 2009 ISBN 0-07-727620-5
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  10. ↑ Kodirov,Sodikdjon A., Shuichi Takizawa, Jamie Joseph, Eric R. Kandel, Gleb P. Shumyatsky, and Vadim Y. Bolshakov. Synaptically released zinc gates long-term potentiation in fear conditioning pathways. PNAS, 10 October 2006. 103(41): 15218-23. doi:10.1073/pnas.0607131103
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  12. ↑ Lua error in package.lua at line 80: module 'strict' not found.
  13. ↑ Lua error in package.lua at line 80: module 'strict' not found.
  14. ↑ Glutamate: Seizures and strokes- PLoS Biol. 2006 November; 4(11): e371. Published online 2006 October 17. doi: 10.1371/journal.pbio.0040371 by author Liza Gross- Courtesy Public Library of Science (2006); PubMed (PMC) of NCBI, Retrieved 2013-16-13
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  16. ↑ Orexin receptor antagonists a new class of sleeping pill, National Sleep Foundation.
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  18. ↑ Schacter, Gilbert and Weger. Psychology.United States of America.2009.Print.
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  20. ↑ 20.0 20.1 20.2 20.3 Lua error in package.lua at line 80: module 'strict' not found.
  21. ↑ 21.0 21.1 21.2 Lua error in package.lua at line 80: module 'strict' not found.
  22. ↑ 22.0 22.1 22.2 Lua error in package.lua at line 80: module 'strict' not found.
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  24. ↑ 24.0 24.1 24.2 24.3 Lua error in package.lua at line 80: module 'strict' not found.
  25. ↑ Lua error in package.lua at line 80: module 'strict' not found.
  26. ↑ Lua error in package.lua at line 80: module 'strict' not found.
  27. ↑ Lua error in package.lua at line 80: module 'strict' not found.
  28. ↑ Lua error in package.lua at line 80: module 'strict' not found.
  29. ↑ Lua error in package.lua at line 80: module 'strict' not found.
  30. ↑ Lua error in package.lua at line 80: module 'strict' not found.
  31. ↑ Lua error in package.lua at line 80: module 'strict' not found.
  32. ↑ Lua error in package.lua at line 80: module 'strict' not found.
  33. ↑ 33.0 33.1 Lua error in package.lua at line 80: module 'strict' not found.
  34. ↑ 34.0 34.1 34.2 Lua error in package.lua at line 80: module 'strict' not found.
     • Figure 1: Schematic of brain CB1 expression and orexinergic neurons expressing OX1 or OX2
     • Figure 2: Synaptic signaling mechanisms in cannabinoid and orexin systems
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  36. ↑ Lua error in package.lua at line 80: module 'strict' not found.
  37. ↑ Lua error in package.lua at line 80: module 'strict' not found.
  38. ↑ Lua error in package.lua at line 80: module 'strict' not found.
  39. ↑ Lua error in package.lua at line 80: module 'strict' not found.
  40. ↑ 40.0 40.1 40.2 40.3 40.4 Lua error in package.lua at line 80: module 'strict' not found.
  41. ↑ Lua error in package.lua at line 80: module 'strict' not found.
  42. ↑ Lua error in package.lua at line 80: module 'strict' not found.
  43. ↑ "General, Organic ans Biological Chemistry Structures of Life" by Karen C. Timberlake p.661
  44. ↑ Leo, J., & Lacasse, J. (2007, October 10). The Media and the Chemical Imbalance Theory of Depression. Retrieved December 1, 2014, from http://psychrights.org/articles/TheMediaandChemicalImbalanceTheoryofDepression.pdf

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