Molecular biology and ontogeny of γ-Aminobutyric acid (GABA) receptors in the mammalian central nervous system

Timothy Simeone, Sean D. Donevan, Jong M. Rho

Research output: Contribution to journalReview article

45 Citations (Scopus)

Abstract

γ-Aminobutyric acid (GABA) is the predominant inhibitory neurotransmitter in the mammalian central nervous system. After release from nerve terminals, GABA binds to at least two classes of postsynaptic receptors (ie, GABAA and GABAB), which are nearly ubiquitous in the brain. GABAA receptors are postsynaptic heteropentameric complexes that display unique physiologic and pharmacologic properties based on subunit composition. Activation of GABAA receptors in mature neurons results in membrane hyperpolarization, which is mediated principally by inward chloride flux, whereas in early stages of brain development, GABAA receptor activation causes depolarization of the postsynaptic membrane. GABAB receptors reside both presynaptically and postsynaptically, exist as heterodimers and are coupled to voltage-dependent ion channels through interactions with heterotrimeric G proteins. This review summarizes the molecular biology and ontogeny of GABAA and GABAB receptors, highlighting some of their putative roles during normal brain development as well as in disease states such as epilepsy.

Original languageEnglish
Pages (from-to)39-48
Number of pages10
JournalJournal of Child Neurology
Volume18
Issue number1
StatePublished - Jan 1 2003

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Aminobutyrates
GABA Receptors
GABA-A Receptors
Molecular Biology
Central Nervous System
gamma-Aminobutyric Acid
Brain
Heterotrimeric GTP-Binding Proteins
Membranes
Ion Channels
Neurotransmitter Agents
Chlorides
Epilepsy
Neurons

All Science Journal Classification (ASJC) codes

  • Clinical Neurology
  • Pediatrics, Perinatology, and Child Health

Cite this

Molecular biology and ontogeny of γ-Aminobutyric acid (GABA) receptors in the mammalian central nervous system. / Simeone, Timothy; Donevan, Sean D.; Rho, Jong M.

In: Journal of Child Neurology, Vol. 18, No. 1, 01.01.2003, p. 39-48.

Research output: Contribution to journalReview article

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