Synaptic inhibition and γ-aminobutyric acid in the mammalian central nervous system

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Abstract

Signal transmission through synapses connecting two neurons is mediated by release of neurotransmitter from the presynaptic axon terminals and activation of its receptor at the postsynaptic neurons. γ-Aminobutyric acid (GABA), non-protein amino acid formed by decarboxylation of glutamic acid, is a principal neurotransmitter at inhibitory synapses of vertebrate and invertebrate nervous system. On one hand glutamic acid serves as a principal excitatory neurotransmitter. This article reviews GABA researches on; (1) synaptic inhibition by membrane hyperpolarization, (2) exclusive localization in inhibitory neurons, (3) release from inhibitory neurons, (4) excitatory action at developmental stage, (5) phenotype of GABA-deficient mouse produced by gene-targeting, (6) developmental adjustment of neural network and (7) neurological/psychiatric disorder. In the end, GABA functions in simple nervous system and plants, and non-amino acid neurotransmitters were supplemented.

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Cortical inhibitory neurons and schizophrenia.

David A. Lewis, Takanori Hashimoto, David W Volk (2005)

Impairments in certain cognitive functions, such as working memory, are core features of schizophrenia. Convergent findings indicate that a deficiency in signalling through the TrkB neurotrophin receptor leads to reduced GABA (gamma-aminobutyric acid) synthesis in the parvalbumin-containing subpopulation of inhibitory GABA neurons in the dorsolateral prefrontal cortex of individuals with schizophrenia. Despite both pre- and postsynaptic compensatory responses, the resulting alteration in perisomatic inhibition of pyramidal neurons contributes to a diminished capacity for the gamma-frequency synchronized neuronal activity that is required for working memory function. These findings reveal specific targets for therapeutic interventions to improve cognitive function in individuals with schizophrenia.

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GABA: a pioneer transmitter that excites immature neurons and generates primitive oscillations.

Yehezkel Ben-Ari, Jean-Luc Gaiarsa, Roman Tyzio … (2007)

Developing networks follow common rules to shift from silent cells to coactive networks that operate via thousands of synapses. This review deals with some of these rules and in particular those concerning the crucial role of the neurotransmitter gamma-aminobuytric acid (GABA), which operates primarily via chloride-permeable GABA(A) receptor channels. In all developing animal species and brain structures investigated, neurons have a higher intracellular chloride concentration at an early stage leading to an efflux of chloride and excitatory actions of GABA in immature neurons. This triggers sodium spikes, activates voltage-gated calcium channels, and acts in synergy with NMDA channels by removing the voltage-dependent magnesium block. GABA signaling is also established before glutamatergic transmission, suggesting that GABA is the principal excitatory transmitter during early development. In fact, even before synapse formation, GABA signaling can modulate the cell cycle and migration. The consequence of these rules is that developing networks generate primitive patterns of network activity, notably the giant depolarizing potentials (GDPs), largely through the excitatory actions of GABA and its synergistic interactions with glutamate signaling. These early types of network activity are likely required for neurons to fire together and thus to "wire together" so that functional units within cortical networks are formed. In addition, depolarizing GABA has a strong impact on synaptic plasticity and pathological insults, notably seizures of the immature brain. In conclusion, it is suggested that an evolutionary preserved role for excitatory GABA in immature cells provides an important mechanism in the formation of synapses and activity in neuronal networks.

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Is there more to GABA than synaptic inhibition?

David Owens, Arnold R. Kriegstein (2002)

In the mature brain, GABA (gamma-aminobutyric acid) functions primarily as an inhibitory neurotransmitter. But it can also act as a trophic factor during nervous system development to influence events such as proliferation, migration, differentiation, synapse maturation and cell death. GABA mediates these processes by the activation of traditional ionotropic and metabotropic receptors, and probably by both synaptic and non-synaptic mechanisms. However, the functional properties of GABA receptor signalling in the immature brain are significantly different from, and in some ways opposite to, those found in the adult brain. The unique features of the early-appearing GABA signalling systems might help to explain how GABA acts as a developmental signal.

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Author and article information

Journal

Journal ID (nlm-ta): Proc Jpn Acad Ser B Phys Biol Sci

Journal ID (iso-abbrev): Proc. Jpn. Acad., Ser. B, Phys. Biol. Sci

Journal ID (publisher-id): PJAB

Title: Proceedings of the Japan Academy. Series B, Physical and Biological Sciences

Publisher: The Japan Academy (Tokyo, Japan )

ISSN (Print): 0386-2208

ISSN (Electronic): 1349-2896

Publication date (Print): 11 April 2013

Volume: 89

Issue: 4

Pages: 139-156

Affiliations

[*1 ]National Institute for Physiological Sciences, Okazaki, Japan.

Author notes

[† ]Correspondence should be addressed: Daimon 3-25-13, Okazaki, Aichi 444-2135, Japan (e-mail: obak37@ 123456email.plala.or.jp ).

(Communicated by Masanori OTSUKA, M.J.A.)

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Publisher ID: pjab-89-139

DOI: 10.2183/pjab.89.139

PMC ID: 3669732

PubMed ID: 23574805

SO-VID: db3ebdbe-b037-43cb-9bda-22ae43bc9861

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This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Synaptic inhibition and γ-aminobutyric acid in the mammalian central nervous system

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Abstract

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The Dynamic Brain

Most cited references 76

Cortical inhibitory neurons and schizophrenia.

GABA: a pioneer transmitter that excites immature neurons and generates primitive oscillations.

Is there more to GABA than synaptic inhibition?

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