Neurotransmitter

Neurotransmitter

Structure of a typical chemical synapse

Neurotransmitters are endogenous chemicals that send out signals across a synapse from one neuron (brain cell) to another 'target' neuron.[1] They are packaged into synaptic vesicles clustered underneath the membrane in the axon terminal located at the presynaptic surface of a synapse. Neurotransmitters are released into and diffused across the synaptic cleft, where they connect to precise receptors in the membrane on the postsynaptic surface of the synapse.[2] Numerous neurotransmitters are synthesized from plentiful and straightforward precursors (such as amino acids), which are willingly available from the diet and only necessitate a small integer of biosynthetic processes to convert them. Neurotransmitters take part in shaping everyday living and functions. Scientists do not yet know precisely how many neurotransmitters exist, but more than 100 chemical messengers have been acknowledged.[3]

The majority of neurotransmitters are about the dimensions of a single amino acid; on the other hand, a quantity of neurotransmitters may have the dimensions of bigger proteins or peptides. A released neurotransmitter is usually obtainable in the synaptic cleft for a little while before it is metabolized by enzymes, pulled back into the presynaptic neuron through reuptake, or bound to a postsynaptic receptor. Furthermore, temporary exposure of the receptor to a neurotransmitter is typically adequate for producing a postsynaptic reaction 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, furthermore, occurs without electrical stimulation. The released neurotransmitter may then travel across the synapse to be detected by and connect with receptors in the postsynaptic neuron. Binding of neurotransmitters may manipulate the postsynaptic neuron in either an inhibitory or excitatory way. This neuron may be linked to many more neurons, and if the full amount of excitatory influences is greater than those of inhibitory influences, the neuron will also "fire". In due course it will generate a new action potential at its axon hillock to discharge neurotransmitters and pass on the information to yet an additional neighboring neuron.[4]


Contents

  • Discovery 1
  • Identification 2
  • Types 3
    • List of neurotransmitters, peptides, and gasotransmitters 3.1
  • Actions 4
    • Excitatory and Inhibitory 4.1
    • Examples of important neurotransmitter actions 4.2
  • Brain neurotransmitter systems 5
  • Drug effects 6
    • Agonists 6.1
      • Drug agonists 6.1.1
    • Antagonists 6.2
      • Drug antagonists 6.2.1
    • Precursors 6.3
      • Catecholamine and trace amine precursors 6.3.1
      • Serotonin precursors 6.3.2
  • Diseases and disorders 7
  • Elimination of neurotransmitters 8
  • Neurotransmitter imbalance 9
  • See also 10
  • References 11
  • External links 12

Discovery

In anticipation of the early 20th century, scientists understood that the preponderance of synaptic communications inside the brain were electrical. Nonetheless, cautious histological examinations by Ramón y Cajal (1852–1934), led to the breakthrough of what is at the moment known as the synaptic cleft, a 20 to 40 nm opening between neurons. The existence of synaptic clefts suggested communications by the use of chemical messengers traversing the synaptic cleft. Additionally, in 1921, German pharmacologist Otto Loewi (1873–1961) long-established that neurons know how to communicate by releasing chemicals. Loewi led a sequence of experiments relating the vagus nerves of frogs and was intelligent enough to manually deliberate the heart rate of frogs by controlling the quantity of saline solution in attendance in the region of the vagus nerve. Upon conclusion of this experiment, Loewi asserted that sympathetic regulations of cardiac function can be mediated through changes in chemical concentrations. Otto Loewi is currently accredited with discovering acetylcholine (ACh)—the first branded neurotransmitter.[5] Some neurons, nevertheless, communicate by means of electrical synapses through the use of gap junctions, which permit specific ions to bypass 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 generate a response in some target.
  3. The same response must be obtained when the chemical is experimentally positioned on the target.
  4. A mechanism must exist for removing the chemical from its place of activation after its work is done.

On the other hand, given advances in pharmacology, genetics, and chemical neuroanatomy, the name "neurotransmitter" can be applied to chemicals that:

  • Transmit messages between neurons using influence on the postsynaptic membrane.
  • Have petite or no end product on membrane voltage, but have a widespread carrying function such as varying the organization of the synapse.
  • Communicate by sending reverse-direction messages that leave a shock on the release or reuptake of transmitters.

The anatomical localization of neurotransmitters is normally determined by means of immunocytochemical techniques, which recognize either the position of either the transmitter substances themselves, or of the enzymes that are implicated in their synthesis. Immunocytochemical techniques have also exposed that countless transmitters, predominantly the neuropeptides, are co-localized, that is, one neuron possibly will release more than one transmitter from its synaptic terminal.[7] An assortment of techniques and experiments such as staining, stimulating, and collecting can be used to categorize neurotransmitters throughout the central nervous system.[8]

Types

There are many ways to pigeonhole neurotransmitters. However, for classification purposes, the most important neurotransmitters are: amino acids, amines (monoamines and other biogenic amines), peptides, and certain soluble gases.

Major neurotransmitters:

In addition, over fifty (50) neuroactive peptides have been revealed and more up to date peptides are brought into being regularly. Many of these are "co-released" by the side of small-molecule transmitter. Nevertheless, in some situations, a peptide is the primary transmitter at a synapse. β-endorphin is a comparatively well known illustration of a peptide neurotransmitter because it engages in exceedingly explicit 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 created in the neural cytoplasm and are instantaneously diffused through the cell membrane into the extracellular fluid and into nearby cells to encourage the manufacturing of second messengers. Soluble gas neurotransmitters are complicated to examine due to their rapid activity and an immediately breaking down process which only lasts for a few seconds.

The most ubiquitous transmitter is glutamate, which is excitatory at well over 90% of the synapses in the human brain [4] followed by Gamma-Aminobutyric Acid, or GABA, which is inhibitory at more than 90% of the synapses that do not use glutamate. Even though other transmitters are used in fewer synapses, they may be very significant functionally: the enormous majority of psychoactive drugs bring to bear their special effects by changing the proceedings of some neurotransmitter systems, over and over again performing through transmitters other than glutamate or GABA. Addictive drugs such as cocaine and amphetamines put forth their effects first and foremost on the dopamine system. The addictive opiate drugs make use of their effects for the most part as functional analogs of opioid peptides, which, in turn, standardize 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 Adrenergic receptor
Small: Monoamine (Phe/Tyr) Epinephrine (adrenaline) Epi 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: 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
Other Anandamide AEA Cannabinoid receptor
Other 2-Arachidonoylglycerol 2-AG Cannabinoid receptor
Other 2-Arachidonyl glyceryl ether 2-AGE Cannabinoid receptor
Other N-Arachidonoyl dopamine NADA Cannabinoid receptor TRPV1
Other Virodhamine Cannabinoid receptor
Other Adenosine triphosphate ATP P2Y12 P2X receptor
Other Adenosine Ado Adenosine receptor

Actions

Neurons create highly structured networks through which nerve impulses—action potentials—journey. Each neuron has 15,000 acquaintances with neighboring neurons. Neurons do notmake contact with with one another except in the case of an electrical synapse through a gap junction. ; as an alternative, neurons work together at synapses- a connection surrounded by two nerve cells consisting of a minuscule opening which impulses pass by a neurotransmitter. A neuron transports information through an action potential. When an action potential arrives at the presynaptic terminal button, it stimulates the release of a neurotransmitter that is then released into the synaptic cleft to fasten onto the receptors of the postsynaptic membrane.

The synthesis, packaging, secretion, and removal of neurotransmitters.


Excitatory and Inhibitory

Neurotransmitters are capable of influencing the function of a neuron through a remarkable number of mechanisms. In its direct proceedings in influencing a neuron’s electrical excitability, however, a neurotransmitter acts in only one of two ways: It influences trans-membrane ion course either to amplify or to reduce the probability that the cell with which it comes in contact will produce an action potential. Therefore, notwithstanding the extensive assortment of synapses, they all communicate messages of only these two types, excitatory or inhibitory, and they are labeled as such. Type I synapses are excitatory in their actions, whereas type II synapses are inhibitory. Each type has a dissimilar manifestation and is to be found on different parts of the neurons under its influence. Each neuron receives thousands of excitatory and inhibitory signals per second.

Type I (excitatory) synapses are classically located on the shafts or the spines of dendrites, while type II (inhibitory) synapses are naturally located on a cell body. In addition, Type I synapses contain round synaptic vesicles, whereas the vesicles of type II synapses are flattened. The substance 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 positions of Type I and Type II synapses separate a neuron into two zones: an excitatory dendritic tree and an inhibitory cell body. From an inhibitory perspective, excitation occurs over the dendrites and spreads to the axon hillock to activate an action potential. If the message is to be blocked, it is best stopped by applying inhibition on the cell body, close to the axon hillock where the action potential originates. An additional method of conceptualizing excitatory–inhibitory interaction is excitation overcoming inhibition, meaning if the cell body is more often than not in an inhibited state, the only way to cause an action potential at the axon hillock is to trim down the cell body’s inhibition. In this “open the gates” approach, the excitatory message can be compared to a racehorse ready to run down the track without the starting gate.[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][13][24]
Noradernergic pathways:
Dopamine system
[13][25][24]
Dopaminergic pathways:
Histamine system
[26]
Histaminergic pathways:
Serotonin system
[22][27][13][24][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][29][13][24]
Cholinergic pathways:

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

  • Brainstem nuclei projections

Forebrain cholinergic nuclei (FCN):
Medial septal nucleus and diagonal band

  • Forebrain 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

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. This works when muscles are at relaxation.[33]

There are two different types of Agonist: Direct-binding Agonist and Indirect-acting Agonist:

  1. Direct-binding Agonist - acts similar to a neurotransmitter in which it directly binds to the receptor site. It allows the recipient to experience drug effects as if they were released directly into the brain. These include dopamine, apomorphine, and nicotine.
  2. Indirect-acting Agonist- which enhances the neurotransmitter actions by stimulating its release while increasing emissions. This includes cocaine.[34]

Drug agonists

"An agonist is a drug or an endogenous substance that binds to a Receptor (it has affinity for the receptor binding site) and produces a biological response (it possesses intrinsic activity). The binding of a drug agonist to the receptor produces an effect that mimics the physiological response observed when an endogenous substance (e.g., hormone, Neurotransmitter) binds to the same receptor. In many cases, the biological response is directly related to the concentration of the agonist available to bind to the receptor. As more agonist is added, the number of receptors occupied increases, as does the magnitude of the response. The potency (strength) of the agonist for producing the physiological response (how much drug is needed to produce the effect) is related to the strength of binding (the affinity) for the receptor and to its intrinsic activity. Most drugs bind to more than one receptor; they have multiple receptor interactions."[35]

Nicotine, found in tobacco, is an agonist for acetylcholine at nicotinic receptors.[36] Opiate agonists include morphine, heroin, hydrocodone, oxycodone, codeine, and methadone. These drugs activate mu opioid receptors that typically respond to endogenous transmitters such as enkephalins. When these receptors are activated, individuals experience euphoria, pain relief, and drowsiness.[36]

Antagonists

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. This works when the muscles are in the phase of contraction.[37]

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-actng Antagonist- drugs that inhibit the release/production of neurotransmitters (i.e., Reserpine).[34]

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 atagonists 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.[38]

Precursors

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.[42] 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.[42][43]

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.[42]

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.[42] This conversion requires vitamin C.[19] 5-hydroxytryptophan (5-HTP), also a precursor for serotonin, is more effective than a placebo.[42]

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.[44]

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. 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.[45]

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. Diseases such as depression and anxiety disorders prescribe patients with medications that directly react with neurotransmitter serotonin and norepinephrine which bind to neuroreceptors.[46]

See also

References

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External links

  • Molecular Expressions Photo Gallery: The Neurotransmitter Collection
  • Brain Neurotransmitters
  • Endogenous Neuroactive Extracellular Signal Transducers
  • Neurotransmitter at the US National Library of Medicine Medical Subject Headings (MeSH)
  • neuroscience for kids website
  • brain explorer website
  • wikibooks cellular neurobiology