Gamma-aminobutyric acid: Difference between revisions

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'''Gamma aminobutyric acid''' (GABA) or <math>\gamma</math>-aminobutyrate, is the major inhibitory [[neurotransmitter]] in the [[central nervous system]].<ref name="isbn0-07-145153-6">{{cite book |author=Katzung, Bertram G. |title=Basic and clinical pharmacology |publisher=McGraw-Hill Medical Publishing Division |location=New York |year=2006 |pages= |isbn=0-07-145153-6 |oclc= |doi=}}</ref>  GABA is produced from the [[amino acid]] glutamate through the action of the enzyme [[glutamate decarboxylase]], and is inactivated by degradation to [[succinate]] in a two step mechanism involving the enzymes [[GABA-glutamate transaminase]] and [[succinate semialdehyde dehydrogenase]].
'''Gamma aminobutyric acid''' (GABA) or <math>\gamma</math>-aminobutyrate, is the major inhibitory [[neurotransmitter]] in the [[central nervous system]].<ref name="isbn0-07-145153-6">{{cite book |author=Katzung, Bertram G. |title=Basic and clinical pharmacology |publisher=McGraw-Hill Medical Publishing Division |location=New York |year=2006 |pages= |isbn=0-07-145153-6 |oclc= |doi=}}</ref>  GABA is produced from the [[amino acid]] glutamate through the action of the enzyme [[glutamate decarboxylase]], and is inactivated by degradation to [[succinate]] in a two step mechanism involving the enzymes [[GABA-glutamate transaminase]] and [[succinate semialdehyde dehydrogenase]].
==Receptors==
GABA<sub>A</sub> is the most prominent.<ref name="G&G_Chapt11">Bloom Floyd E, "Chapter 12.  Neurotransmission and the Central Nervous System" (Chapter). Brunton LL,  Lazo JS, Parker KL: Goodman & Gilman's The Pharmacological Basis of  Therapeutics, 11e:  http://www.accessmedicine.com/content.aspx?aID=937279.</ref> Many medications, many neuroactive drugs (see Chapters 16 and 22), "[[benzodiazepine]]s, [[barbiturate]]s, [[ethanol]], anesthetic steroids,  and [[volatile anesthetic]]s", act on the GABA<sub>A</sub> receptor.<ref name="G&G_Chapt11"/>
GABA<sub>B</sub> "function as autoreceptors, inhibiting GABA release".<ref name="G&G_Chapt11"/>
GABA<sub>C</sub> is less widely distributed and is in the [[retina]], [[spinal cord]], superior colliculus, and [[pituitary gland]]. GABA<sub>C</sub> receptors are not affected by the agonist [[baclofen]] or the modulators [[benzodiazepine]]s and [[barbiturate]]s.<ref name="G&G_Chapt11"/>


==Role in clinical pharmacology==
==Role in clinical pharmacology==
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GABA modulators have various roles.
GABA modulators have various roles.


===Gamma-aminobutyric acid (GABA) agonists===
===Gamma-aminobutyric acid (GABA) (physiologic) agonists===
Drugs that increase the effect or secretion of GABA are called GABAergic, such as [[baclofen]].
Drugs that increase the effect or secretion of GABA are called GABAergic, such as [[baclofen]].


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Pyrazolopyrimidines
Pyrazolopyrimidines
* [[Zaleplon]] (Sonata; Starnoc). May have similar abuse potential to [[benzodiazepam]]s.<ref name="pmid10445371">{{cite journal| author=Rush CR, Frey JM, Griffiths RR| title=Zaleplon and triazolam in humans: acute behavioral effects and abuse potential. | journal=Psychopharmacology (Berl) | year= 1999 | volume= 145 | issue= 1 | pages= 39-51 | pmid=10445371  
* [[Zaleplon]] (Sonata; Starnoc). May have similar abuse potential to [[benzodiazepam]]s.<ref name="pmid10445371">{{cite journal| author=Rush CR, Frey JM, Griffiths RR| title=Zaleplon and triazolam in humans: acute behavioral effects and abuse potential. | journal=Psychopharmacology (Berl) | year= 1999 | volume= 145 | issue= 1 | pages= 39-51 | pmid=10445371  
| url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=10445371 }} <!--Formatted by http://sumsearch.uthscsa.edu/cite/--></ref>
| url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=10445371 }}></ref>


==References==
==References==
<references/>
<references/>

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Synthesis and degradation of GABA.

Gamma aminobutyric acid (GABA) or -aminobutyrate, is the major inhibitory neurotransmitter in the central nervous system.[1] GABA is produced from the amino acid glutamate through the action of the enzyme glutamate decarboxylase, and is inactivated by degradation to succinate in a two step mechanism involving the enzymes GABA-glutamate transaminase and succinate semialdehyde dehydrogenase.

Receptors

GABAA is the most prominent.[2] Many medications, many neuroactive drugs (see Chapters 16 and 22), "benzodiazepines, barbiturates, ethanol, anesthetic steroids, and volatile anesthetics", act on the GABAA receptor.[2]

GABAB "function as autoreceptors, inhibiting GABA release".[2]

GABAC is less widely distributed and is in the retina, spinal cord, superior colliculus, and pituitary gland. GABAC receptors are not affected by the agonist baclofen or the modulators benzodiazepines and barbiturates.[2]

Role in clinical pharmacology

For more information, see: GABA modulator.

GABA modulators have various roles.

Gamma-aminobutyric acid (GABA) (physiologic) agonists

Drugs that increase the effect or secretion of GABA are called GABAergic, such as baclofen.

Many sedatives work by increasing receptiveness of GABAA receptors.

Barbituates

Barbituates are GABAergic by increasing receptiveness of the GABAA receptors. Barbituates do this by increasing the duration of openings of channels in the cell membrane.[1]

  • Phenobarbital

Gabapentin & Pregabalin

Gabapentin and pregabalinare both analogs that are agonists of GABA.

Nonselective BZ1 and BZ2 agonists

Benzodiazepines are also nonselective GABAergic by increasing receptiveness of the GABAA receptors. However, benzodiazepines do this by increasing the frequency of openings of channels in the cell membrane.[1]

Benzodiazepine receptors are BZ1 and BZ2.

BZ1 selective agonists

Cyclopyrrolones / Piperazines

Imidazopyridines

Pyrazolopyrimidines

References

  1. ↑ 1.0 1.1 1.2 Katzung, Bertram G. (2006). Basic and clinical pharmacology. New York: McGraw-Hill Medical Publishing Division. ISBN 0-07-145153-6. 
  2. ↑ 2.0 2.1 2.2 2.3 Bloom Floyd E, "Chapter 12. Neurotransmission and the Central Nervous System" (Chapter). Brunton LL, Lazo JS, Parker KL: Goodman & Gilman's The Pharmacological Basis of Therapeutics, 11e: http://www.accessmedicine.com/content.aspx?aID=937279.
  3. ↑ Rush CR, Frey JM, Griffiths RR (1999). "Zaleplon and triazolam in humans: acute behavioral effects and abuse potential.". Psychopharmacology (Berl) 145 (1): 39-51. PMID 10445371. >
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