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Neurotransmission

by Ricardo Cruciani, MD, PhD

A neuron generates and propagates an action potential along its axon, then transmits this signal across a synapse by releasing neurotransmitters, which trigger a reaction in another neuron or an effector cell (eg, muscle cells, most exocrine and endocrine cells). The signal may stimulate or inhibit the receiving cell, depending on the neurotransmitter and receptor involved.

In the CNS, interconnections are complex. An impulse from one neuron to another may pass from axon to cell body, axon to dendrite (a neuron’s receiving branches), cell body to cell body, or dendrite to dendrite. A neuron can simultaneously receive many impulses—excitatory and inhibitory—from other neurons and integrate simultaneous impulses into various patterns of firing.

Propagation

Action potential propagation along an axon is electrical, caused by the exchanges of Na + and K + ions across the axonal membrane. A particular neuron generates the same action potential after each stimulus, conducting it at a fixed velocity along the axon. Velocity depends on axonal diameter and degree of myelination and ranges from 1 to 4 m/sec in small unmyelinated fibers to 75 m/sec in large myelinated ones. Propagation speed is higher in myelinated fibers because the myelin cover has regular gaps (nodes of Ranvier) where the axon is exposed. The electrical impulse jumps from one node to the next, skipping the myelinated section of the axon. Thus, disorders that alter the myelin cover (eg, multiple sclerosis) interfere with impulse propagation, causing various neurologic symptoms.

Transmission

Impulse transmission is chemical, caused by release of specific neurotransmitters from the nerve ending (terminal). Neurotransmitters diffuse across the synaptic cleft and bind briefly to specific receptors on the adjoining neuron or effector cell. Depending on the receptor, the response may be excitatory or inhibitory.

One type of synapse, the electrical synapse, does not involve neurotransmitters; ion channels directly connect the cytoplasm of the presynaptic and postsynaptic neurons. This type of transmission is the fastest.

The nerve cell body produces enzymes that synthesize most neurotransmitters, which are stored in vesicles at the nerve terminal (see see Figure: Neurotransmission). The amount in one vesicle (usually several thousand molecules) is a quantum. A membrane action potential arriving at the terminal opens axonal Ca channels; Ca inflow releases neurotransmitter molecules from many vesicles by fusing the vesicle membranes to the nerve terminal membrane. Membrane fusion generates an opening through which the molecules are expelled into the synaptic cleft via exocytosis.

Neurotransmission

Action potentials open the axonal Ca channels (not shown). Ca ++ activates release of neurotransmitters (NT) from vesicles where they are stored. NT molecules fill the synaptic cleft. Some bind to postsynaptic receptors, initiating a response. The others are pumped back into the axon and stored or diffuse into the surrounding tissues.

The amount of neurotransmitters in the terminal is typically independent of nerve activity and kept relatively constant by modifying uptake of neurotransmitter precursors or the activity of enzymes involved in neurotransmitter synthesis or destruction. Stimulation of presynaptic receptors can decrease presynaptic neurotransmitter synthesis, and blockade can increase it.

The neurotransmitter-receptor interaction must be terminated quickly to allow rapid, repeated activation of receptors. One of the following can happen to neurotransmitters that have interacted with receptors:

  • They can be quickly pumped back into the presynaptic nerve terminals by active, ATP-dependent processes (reuptake).

  • They can be destroyed by enzymes near the receptors.

  • They can diffuse into the surrounding area and be removed.

Neurotransmitters taken up by the nerve terminals are repackaged in vesicles for reuse.

Receptors

Neurotransmitter receptors are protein complexes that span the cell membrane. Their nature determines whether a given neurotransmitter is excitatory or inhibitory. Receptors that are continuously stimulated by neurotransmitters or drugs become desensitized (downregulated); those that are not stimulated by their neurotransmitter or are chronically blocked by drugs become supersensitive (upregulated). Downregulation or upregulation of receptors strongly influences the development of tolerance and physical dependence. These concepts are particularly important in organ or tissue transplantation, in which denervation deprives receptors of their neurotransmitter. Withdrawal symptoms can be explained at least in part by a rebound phenomenon due to altered receptor affinity or density.

Most neurotransmitters interact primarily with postsynaptic receptors, but some receptors are located on presynaptic neurons, providing fine control of neurotransmitter release.

One family of receptors, termed ionotropic receptors (eg, N -methyl- d -glutamate, kinate-quisqualate, nicotinic acetylcholine, glycine, and γ-aminobutyric acid [GABA] receptors), consist of ion channels that open when bound to the neurotransmitter and effect a very rapid response. In the other family, termed metabotropic receptors (eg, serotonin, α- and β-adrenergic, and dopaminergic receptors), neurotransmitters interact with G proteins and activate another molecule (2nd messenger such as cAMP) that catalyzes a chain of events through protein phosphorylation Ca mobilization, or both; cellular changes mediated by 2nd messengers are slower and permit finer tuning of the rapid ionotropic neurotransmitter response. Far more neurotransmitters activate specific receptors than 2nd messengers.

Major Neurotransmitters and Receptors

At least 100 substances can act as neurotransmitters; about 18 are of major importance. Several occur in slightly different forms.

Glutamate and aspartate

These amino acids are the major excitatory neurotransmitters in the CNS. They occur in the cortex, cerebellum, and spinal cord. In neurons, synthesis of nitric oxide (NO) increases in response to glutamate. Excess glutamate can be toxic, increasing intracellular Ca, free radicals, and proteinase activity. These neurotransmitters may contribute to tolerance to opioid therapy and mediate hyperalgesia.

Glutamate receptors are classified as NMDA ( N -methyl- d -aspartate) receptors and non-NMDA receptors. Phencyclidine (PCP, also known as angel dust) and memantine (used to treat Alzheimer’s disease) bind to NMDA receptors.

GABA

GABA is the major inhibitory neurotransmitter in the brain. It is an amino acid derived from glutamate, which is decarboxylated by glutamate decarboxylase. After interaction with its receptors, GABA is actively pumped back into nerve terminals and metabolized. Glycine, which resembles GABA in its action, occurs principally in interneurons (Renshaw cells) of the spinal cord and in circuits that relax antagonist muscles.

GABA receptors are classified as GABA A (activating chloride channels) and GABA B (potentiating cAMP formation). GABA A receptors are the site of action for several neuroactive drugs, including benzodiazepines, barbiturates, picrotoxin, and muscimol. GABA B receptors are activated by baclofen, used to treat muscle spasms (eg, in multiple sclerosis).

Serotonin

Serotonin (5-hydroxytryptamine, or 5-HT) is generated by the raphe nucleus and midline neurons of the pons and upper brain stem. Tryptophan is hydroxylated by tryptophan hydroxylase to 5-hydroxytryptophan, then decarboxylated to serotonin. Serotonin levels are controlled by the uptake of tryptophan and intraneuronal monoamine oxidase (MAO), which breaks down serotonin. Ultimately, serotonin is excreted in the urine as 5-hydroxyindoacetic acid or 5-HIAA.

Serotoninergic (5-HT) receptors (with at least 15 subtypes) are classified as 5-HT 1 (with 4 subtypes), 5-HT 2 , and 5-HT 3 . Selective serotonin receptor agonists (eg, sumatriptan) can abort migraines.

Acetylcholine

Acetylcholine is the major neurotransmitter of the bulbospinal motor neurons, autonomic preganglionic fibers, postganglionic cholinergic (parasympathetic) fibers, and many neurons in the CNS (eg, basal ganglia, motor cortex). It is synthesized from choline and acetyl coenzyme A by choline acetyltransferase, and its action is rapidly terminated via local hydrolysis to choline and acetate by acetylcholinesterase. Acetylcholine levels are regulated by choline acetyltransferase and by choline uptake. Levels of this neurotransmitter are decreased in patients with Alzheimer’s disease.

Cholinergic receptors are classified as nicotinic N 1 (in the adrenal medulla and autonomic ganglia) or N 2 (in skeletal muscle) or muscarinic M 1 through M 5 (widely distributed in the CNS). M 1 occurs in the autonomic nervous system, striatum, cortex, and hippocampus; M 2 occurs in the autonomic nervous system, heart, intestinal smooth muscle, hindbrain, and cerebellum.

Dopamine

Dopamine interacts with receptors on some peripheral nerve fibers and many central neurons (eg, in the substantia nigra, midbrain, ventral tegmental area, and hypothalamus). The amino acid tyrosine is taken up by dopaminergic neurons and converted by tyrosine hydroxylase to 3,4-dihydroxyphenylalanine (dopa), which is decarboxylated by aromatic- l -amino-acid decarboxylase to dopamine. After release and interaction with receptors, dopamine is actively pumped back (reuptake) into the nerve terminal. Tyrosine hydroxylase and MAO (which breaks down dopamine) regulate dopamine levels in nerve terminals.

Dopaminergic receptors are classified as D 1 through D 5 . D 3 and D 4 receptors play a role in thought control (limiting the negative symptoms of schizophrenia); D 2 receptor activation controls the extrapyramidal system. However, receptor affinity does not predict functional response (intrinsic activity); eg, ropinirole, which has high affinity for the D 3 receptor, has intrinsic activity via activation of D 2 receptors.

Norepinephrine

Norepinephrine is the neurotransmitter of most postganglionic sympathetic fibers and many central neurons (eg, in the locus caeruleus and hypothalamus). The precursor tyrosine is converted to dopamine, which is hydroxylated by dopamine β-hydroxylase to norepinephrine. After release and interaction with receptors, some norepinephrine is degraded by catechol O -methyltransferase (COMT), and the remainder is actively taken back into the nerve terminal, where it is degraded by MAO. Tyrosine hydroxylase, dopamine β-hydroxylase, and MAO regulate intraneuronal norepinephrine levels.

Adrenergic receptors are classified as α 1 (postsynaptic in the sympathetic system), α 2 (presynaptic in the sympathetic system and postsynaptic in the brain), β 1 (in the heart), or β 2 (in other sympathetically innervated structures).

Endorphins and enkephalins

Endorphins and enkephalins are opioids. Endorphins are large polypeptides that activate many central neurons (eg, in the hypothalamus, amygdala, thalamus, and locus caeruleus). The cell body contains a large polypeptide called pro-opiomelanocortin, the precursor of α-, β-, and γ-endorphins. This polypeptide is transported down the axon and cleaved into fragments; one is β-endorphin, contained in neurons that project to the periaqueductal gray matter, limbic structures, and major catecholamine-containing neurons in the brain. After release and interaction with receptors, β-endorphin is hydrolyzed by peptidases.

Met-enkephalin and leu-enkephalin are small polypeptides present in many central neurons (eg, in the globus pallidus, thalamus, caudate, and central gray matter). Their precursor, proenkephalin, is formed in the cell body, then split by specific peptidases into the active peptides. These substances are also localized in the spinal cord, where they modulate pain signals. The neurotransmitters of pain signals in the posterior horn of the spinal cord are glutamate and substance P. Enkephalins decrease the amount of neurotransmitter released and hyperpolarize (make more negative) the postsynaptic membrane, reducing the generation of action potentials and pain perception at the level of the postcentral gyrus. After release and interaction with peptidergic receptors, enkephalins are hydrolyzed into smaller, inactive peptides and amino acids. Rapid inactivation of exogenous enkephalins prevents these substances from being clinically useful. More stable molecules (eg, morphine ) are used as analgesics instead.

Endorphin-enkephalin (opioid) receptors are classified as μ 1 and μ 2 (affecting sensorimotor integration and analgesia), δ 1 and δ 2 (affecting motor integration, cognitive function, and analgesia), and κ 1 , κ 2 , and κ 3 (affecting water balance regulation, analgesia, and food intake). σ-Receptors, currently classified as nonopioid and mostly localized in the hippocampus, bind PCP. New data suggest the presence of many more receptor subtypes, with pharmacologic implications. Components of the molecular precursor to the receptor protein can be rearranged during receptor synthesis to produce several receptor variants (eg, 27 splice variants of the μ opioid receptor). Also, 2 receptors can combine (dimerize) to form a new receptor.

Other neurotransmitters

Dynorphins are a group of 7 peptides with similar amino acid sequences. They, like enkephalins, are opioids.

Substance P, a peptide, occurs in central neurons (in the habenula, substantia nigra, basal ganglia, medulla, and hypothalamus) and is highly concentrated in the dorsal root ganglia. Its release is triggered by intense afferent painful stimuli. It modulates the neural response to pain and mood; it modulates nausea and vomiting through the activation of NK1A receptors that are localized in the brain stem.

Nitric oxide (NO) is a labile gas that mediates many neuronal processes. It is generated from arginine by NO synthase. Neurotransmitters that increase intracellular Ca ++ (eg, substance P, glutamate, acetylcholine) stimulate NO synthesis in neurons that express NO synthetase. NO may be an intracellular messenger; it may diffuse out of a cell into a 2nd neuron and produce physiologic responses (eg, long-term potentiation [strengthening of certain presynaptic and postsynaptic responses—a form of learning]) or enhance glutamate (NMDA-receptor–mediated) neurotoxicity (eg, in Parkinson’s disease, stroke, or Alzheimer’s disease).

Substances with less firmly established roles in neurotransmission include histamine, vasopressin , vasoactive intestinal peptide, carnosine, bradykinin, cholecystokinin, bombesin, somatostatin, corticotropin-releasing factor, neurotensin, and possibly adenosine .

Disorders Associated With Defects in Neurotransmission

Disorders or substances that alter the production, release, reception, breakdown, or reuptake of neurotransmitters or that change the number and affinity of receptors can cause neurologic or psychiatric symptoms and cause disease (see Examples of Disorders Associated With Defects in Neurotransmission). Drugs that modify neurotransmission can alleviate many of these disorders (eg, Parkinson’s disease, depression).

Examples of Disorders Associated With Defects in Neurotransmission

Disorder

Pathophysiology

Treatment

Neurotransmitter imbalance

Alzheimer’s disease

Extracellular β-amyloid deposits, intracellular neurofibrillary tangles, and senile plaques, particularly in the limbic system (eg, hippocampus), in the association area of the cortex, and in neurons that synthesize and use acetylcholine (eg, in the basal nucleus of Meynert and its wide projections to the cortex)

Cholinesterase inhibitors (donepezil, rivastigmine, galantamine) delay synaptic degradation of acetylcholine and thus modestly improve cognitive function and memory.

Memantine, an NMDA-receptor antagonist, may slow progression of the disease and increase autonomy.

Anxiety

May reflect reduced activity of GABA, perhaps due to imbalance of endogenous inhibitors, stimulators of the GABA receptor, or both

May also involve imbalances in norepinephrine and 5-HT responses

Benzodiazepines increase the probability of opening Cl channels modulated by GABA through GABA A receptor activation.

SSRIs are the drugs of choice for long-term treatment because tolerance to benzodiazepines can develop.

Autism

Possible hyperserotonemia, which occurs in 30–50% of autistic people, with no evidence of central 5-HT abnormalities

SSRIs and risperidone may be helpful.

Brain injury

Injury (eg, trauma, hypoxia, prolonged seizures) stimulating excessive release of excitatory neurotransmitters (eg, glutamate) and accumulation of intracellular Ca ++ , which contribute to neuronal death

In experimental models of ischemia and injury, Ca channel blockers, glycine, and older NMDA-receptor antagonists (eg, dextromethorphan, ketamine) may reduce the extent of neuronal loss, but these drugs are not effective in people.

Memantine, a newer NMDA-receptor antagonist, is under study.

Depression

Complex abnormalities in cholinergic, catecholaminergic (noradrenergic, dopaminergic) and serotonergic (5-HT) transmission

Possible involvement of other hormones and neuropeptides (eg, substance P, dopamine, acetylcholine, GABA)

Antidepressants downregulate receptors indirectly or directly by inhibiting reuptake of 5-HT (as with SSRIs) and norepinephrine or dopamine or by blocking MAO.

Blockade of 5-HT 2A/2C (a type of 5-HT receptor abundant in the prefrontal area) may increase the efficacy of SSRIs (eg, trazodone).

Seizure disorders

Seizures consisting of sudden synchronous high-frequency firing by localized groups of neurons in certain brain areas, perhaps caused by increased activity of glutamate or reduced activity of GABA

Phenytoin, lamotrigine, carbamazepine, valproate, topiramate, and some other anticonvulsants (eg, zonisamide, oxcarbazepine) stabilize voltage-dependent Na channels.

Ethosuximide and gabapentin decrease certain Ca currents.

Phenytoin also reduces excessive neurotransmitter release.

Lamotrigine may decrease levels of glutamate and aspartate.

Phenobarbital and benzodiazepines enhance GABA activation by affecting the GABA A receptor–Cl channel complex.

Tiagabine blocks GABA glial uptake.

Valproate increases levels of GABA.

Topiramate increases GABA activity.

Huntington’s disease (chorea)

Major neuronal damage in the cortex and striatum due to polyglutamine expansion (encoded by CAG repeat), produced by an abnormal gene on chromosome 4 (the abnormal gene overproduces the protein huntingtin, which may combine with molecules that induce excessive stimulation of cells by excitatory amino acid neurotransmitters such as glutamate)

No specific treatment exists, but drugs that block NMDA receptors may block the toxic effects of excess glutamate.

GABA-mimetic drugs are ineffective.

Mania

Increased norepinephrine and dopamine activity, reduced 5-HT levels, and abnormal glutamate neurotransmission

Lithium is the traditional first choice. It reduces norepinephrine release and increases 5-HT synthesis.

Valproate and lamotrigine are beneficial, possibly by normalizing glutamate transmission.

Topiramate blocks voltage-dependent Na channels, augments GAB A activity at some subtypes of the GABA A receptor, antagonizes the AMPA/kainate subtype of the glutamate receptor, and inhibits the carbonic anhydrase enzyme, particularly isozymes II and IV.

Gabapentin is thought to bind to the α2δ subunit (1 and 2) of the voltage-dependent Ca channel in the CNS.

Carbamazepine and oxcarbazepine stabilize voltage dependent Na+ channels.

Neuroleptic malignant syndrome

Blockage of dopamine (D 2 ) receptors by drugs (eg, antipsychotic drugs, methylphenidate) or abrupt withdrawal of a dopaminergic agonist, resulting in muscle rigidity, fever, change in mental status, and autonomic instability

Treatment with a D 2 agonist (eg, bromocriptine) reverses the disordered neurotransmission.

Other drugs are also used as needed (eg, dantrolene, a direct muscular blocker, is used to block the muscle spasms).

Pain

Tissue injury, which causes release of substance P and glutamate in the posterior horn of the spinal cord and release of other macromolecules that mediate pain signals, such as calcitonin gene-related protein, neurokinin A, and bradykinin, which are localized primarily in the lamina II and IV of the spinal cord

Further modulation of these signals by endorphins (in the spinal cord) and by 5-HT and norepinephrine (in the descending pathways that originate in the brain)

NSAIDs inhibit prostaglandin synthesis selectively (with COX-2 inhibitors—eg, celecoxib, parecoxib) or nonselectively (with COX-1 and -2 inhibitors—eg, ibuprofen, naproxen) and reduce pain impulse formation.

Opioid analgesics (eg, morphine) activate endorphin-enkephalin (μ, δ, and κ) receptors, reducing pain impulse transmission.

Parkinsonism

Inhibition of the dopaminergic system due to blockage of dopaminergic receptors by antipsychotic drugs

Anticholinergic drugs reduce cholinergic activity and restore balance between cholinergic and dopaminergic systems.

Parkinson’s disease

Loss of dopaminergic neurons of the pars compacta in the substantia nigra and other areas, with reduced levels of dopamine and metenkephalin, altering the dopamine/acetylcholine balance and resulting in striatal acetylcholine overactivity

l -Dopa reaches the synaptic cleft, is taken up by the axon, and is decarboxylated to dopamine, which is secreted into the cleft to activate dendritic dopamine receptors. Amantadine increases the presynaptic release of dopamine; dopamine agonists stimulate dopamine receptors, although bromocriptine, pramipexole, and ropinirole bind only to D 2 , D 3 , and D 4 dopamine receptor subtypes.

Anticholinergic drugs reduce activity of the cholinergic system, restoring the balance of dopamine and acetylcholine.

MAO-B inhibitors prevent reuptake of dopamine, increasing its levels. Selegiline, an MAO-B inhibitor, blocks dopamine breakdown and thus prolongs the response to levodopa and allows the dosage of carbidopa/levodopa to be reduced.

Catechol O -methyltransferase (COMT) inhibitors also inhibit dopamine breakdown.

Schizophrenia

Increased presynaptic release, synthesis of dopamine, sensitivity or density of postsynaptic dopamine receptors, or a combination

Antipsychotic drugs block dopamine receptors and reduce dopaminergic overactivity to normal.

Haloperidol preferentially blocks D 2 and D 3 receptors (high affinity) and D 4 receptors (low affinity) in mesocortical areas.

Clozapine has a high affinity for binding D 4 and 5-HT 2 receptors, suggesting 5-HT system involvement in the pathogenesis of schizophrenia and its response to treatment. Clozapine has a significant risk of leukopenia.

Olanzapine and risperidone, similar to haloperidol, also have high affinity for 5-HT 2 and D 2 receptors.

Tardive dyskinesia

Hypersensitive dopamine receptors due to chronic blockade by antipsychotic drugs

Reducing doses of antipsychotics may reduce hypersensitivity of dopamine receptors; however, in some cases, changes can be irreversible.

Normal neurotransmitters but nonfunctional receptors

Myasthenia gravis

Reflects inactivation of acetylcholine receptors and postsynaptic histochemical changes at the neuromuscular junction due to autoimmune reactions

Anticholinesterase drugs inhibit acetylcholinesterase, increase acetylcholine levels at the junction, and stimulate remaining receptors, increasing muscle activity.

Decreased neuronal uptake of neurotransmitters

Amyotrophic lateral sclerosis

Destruction of upper and lower motor neurons, possibly caused in part by glutamate neurotoxicity

Riluzole, which inhibits glutamate transmission, modestly extends survival.

Normal neurotransmitters but ion channel defects

Episodic ataxias

Defective voltage-gated K channels, causing distal rippling and incoordination (myokymia)

Treatment with acetazolamide is effective in some types of episodic ataxia.

Hyperkalemic periodic paralysis

Decreased Na channel inactivation

Severe attacks may be terminated by Ca gluconate, glucose, and insulin.

Hypokalemic periodic paralysis

Defective voltage-gated Ca channels

Acute attacks can be terminated by K salts.

Acetazolamide is effective for prevention.

Lambert-Eaton syndrome*

Antibodies that decrease presynaptic release of acetylcholine

Corticosteroids, 3,4-diaminopyridine (DAP), guanidine, IVIG, and plasmapheresis can be helpful.

Paramyotonia congenita

Defective voltage-gated Na channels, causing cold-induced myotonia and episodic weakness

Mexiletine (a Na channel blocker) and acetazolamide (a carbonic anhydrase inhibitor) may be helpful.

Rasmussen’s encephalitis

Postviral production of antibodies to glutamate receptors, affecting glutamate-gated channels

Most distinctive form of epilepsia partialis continua

Corticosteroids and antiviral drugs are usually ineffective.

Functional hemispherectomy can control seizures if spontaneous remission does not occur.

Startle disease (hyperexplexia, stiff baby syndrome)

Mutation in the gene for the α1 subunit of the glycine-gated channel

Characterized by stiffness, nocturnal myoclonus, and an exaggerated startle reflex, with hyperreflexia and falling

Clonazepam or certain other anticonvulsants (eg, phenytoin, phenobarbital, diazepam, valproate) may result in improvement.

Poisoning

Botulism

Inhibition of acetylcholine release from motor neurons by toxin from Clostridium botulinum

No specific drug therapy exists.

Tiny amounts of the toxin are used to treat certain dystonias, spasticity, neuropathic pain, and migraines or cosmetically to reduce skin wrinkles.

Mushroom poisoning

Amanita muscaria: Contains ibotenic acid (which has effects similar to those of glutamate) and a metabolite similar to muscimol (which has effects similar to those of GABA)

Inocybe and Clitocybe spp: Stimulation of muscarinic receptors by muscarine and related compounds

Treatment is supportive because no drugs reverse the effects on neurotransmission.

Atropine helps reverse muscarinic manifestations.

Organophosphates

Irreversible inhibition of acetylcholinesterase and marked increase in acetylcholine levels in synaptic cleft

Pralidoxime removes toxin from acetylcholinesterase and helps reverse nicotinic as well as muscarinic manifestations.

Atropine helps rapidly reverse muscarinic effects.

Snake venom from Bungarus multicinctus (Taiwanese banded krait)

Blocks acetylcholine receptors at neuromuscular junction by α- Bungarus toxin

Antivenom appears to be effective and is available.

*Eaton-Lambert syndrome is an antibody-mediated paraneoplastic syndrome that typically occurs in small cell lung cancer. It can be present before the tumor manifests.

CRF = corticotropin (ACTH)-releasing factor; GABA =γ-aminobutyric acid; 5-HT = serotonin; IVIG = IV immune globulin; MAO = monoamine oxidase; MAO-B = MAO type B; NMDA = N -methyl- d -aspartate; PIP 2 = phosphatidylinositol 4,5-bisphosphate.

Resources In This Article

Drugs Mentioned In This Article

  • Drug Name
    Select Trade
  • NAMENDA
  • LIORESAL
  • IMITREX
  • No US brand name
  • REQUIP
  • LEVOPHED
  • DURAMORPH PF, MS CONTIN
  • R-GENE 10
  • ADENOCARD
  • H.P. ACTHAR GEL
  • VASOSTRICT
  • NEURONTIN
  • DIAMOX
  • RAZADYNE
  • ADVIL, MOTRIN IB
  • ATROPEN
  • PROTOPAM CHLORIDE
  • KETALAR
  • RILUTEK
  • EXELON
  • TOPAMAX
  • OLEPTRO
  • ZARONTIN
  • RISPERDAL
  • ALEVE, NAPROSYN
  • HALDOL
  • KLONOPIN
  • ARICEPT
  • DELSYM
  • LAMICTAL
  • MIACALCIN
  • VALIUM
  • ZYPREXA
  • LODOSYN
  • ELDEPRYL
  • TRILEPTAL
  • ZONEGRAN
  • CLOZARIL
  • PARLODEL
  • DILANTIN
  • DANTRIUM
  • GABITRIL
  • MIRAPEX
  • CONCERTA, RITALIN
  • LITHOBID
  • CELEBREX
  • TEGRETOL

* This is a professional Version *