POSTNATAL MATURATION OF GAMMA-AMINOBUTYRIC ACID(A AND B)-MEDIATED INHIBITION IN THE CA3 HIPPOCAMPAL REGION OF THE RAT

Jean-Luc Gaiarsa, Heather McLean, Patrice Congar, Xavier Leinekugel, Rustem Khazipov, Vadim Tseeb, Yehezkel Ben-Ari
J. Neurobiol.. 1995-03-01; 26(3): 339-349
DOI: 10.1002/neu.480260306

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1. J Neurobiol. 1995 Mar;26(3):339-49.

Postnatal maturation of gamma-aminobutyric acidA and B-mediated inhibition in the
CA3 hippocampal region of the rat.

Gaiarsa JL(1), McLean H, Congar P, Leinekugel X, Khazipov R, Tseeb V, Ben-Ari Y.

Author information:
(1)Institut National de la Santé et de la Recherche Médicale, U29, Hôpital de
Port-Royal, Paris, France.

In the adult central nervous system, GABAergic synaptic inhibition is known to
play a crucial role in preventing the spread of excitatory glutamatergic
activity. This inhibition is achieved by a membrane hyperpolarization through the
activation of postsynaptic gamma-aminobutyric acidA (GABAA) and GABAB receptors.
In addition, GABA also depress transmitter release acting through presynaptic
GABAB receptors. Despite the wealth of data regarding the role of GABA in
regulating the degree of synchronous activity in the adult, little is known about
GABA transmission during early stages of development. In the following we report
that GABA mediates most of the excitatory drive at early stages of development in
the hippocampal CA3 region. Activation of GABAA receptors induces a
depolarization and excitation of immature CA3 pyramidal neurons and increases
intracellular Ca2+ ([Ca2+]i)] during the first postnatal week of life. During the
same developmental period, the postsynaptic GABAB-mediated inhibition is poorly
developed. In contrast, the presynaptic GABAB-mediated inhibition is well
developed at birth and plays a crucial role in modulating the postsynaptic
activity by depressing transmitter release at early postnatal stages. We have
also shown that GABA plays a trophic role in the neuritic outgrowth of cultured
hippocampal neurons.

DOI: 10.1002/neu.480260306
PMID: 7775967 [Indexed for MEDLINE]


Auteurs Bordeaux Neurocampus