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 language | English |
|---|---|
| Pages (from-to) | 39-48 |
| Number of pages | 10 |
| Journal | Journal of Child Neurology |
| Volume | 18 |
| Issue number | 1 |
| State | Published - Jan 1 2003 |
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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 journal › Review article
}
TY - JOUR
T1 - Molecular biology and ontogeny of γ-Aminobutyric acid (GABA) receptors in the mammalian central nervous system
AU - Simeone, Timothy
AU - Donevan, Sean D.
AU - Rho, Jong M.
PY - 2003/1/1
Y1 - 2003/1/1
N2 - 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.
AB - 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.
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M3 - Review article
VL - 18
SP - 39
EP - 48
JO - Journal of Child Neurology
JF - Journal of Child Neurology
SN - 0883-0738
IS - 1
ER -