Modulation of GABAergic transmission by endogenous glutamate in the rat supraoptic nucleus

Richard Piet, Renée Bonhomme, Dionysia T. Theodosis, Dominique A. Poulain, Stéphane H. R. Oliet
European Journal of Neuroscience. 2003-05-01; 17(9): 1777-1785
DOI: 10.1046/j.1460-9568.2003.02611.x

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1. Eur J Neurosci. 2003 May;17(9):1777-85.

Modulation of GABAergic transmission by endogenous glutamate in the rat
supraoptic nucleus.

Piet R(1), Bonhomme R, Theodosis DT, Poulain DA, Oliet SH.

Author information:
(1)INSERM U378, Institut François Magendie, 1, rue Camille St-Saëns, 33077
Bordeaux Cedex, France.

The presence of group III metabotropic glutamate receptors on GABAergic terminals
in the supraoptic nucleus suggests that the level of glutamate in the
extracellular space may regulate synaptic strength at inhibitory synapses. To
test this hypothesis we examined the consequences of increasing ambient glutamate
on GABA-mediated synaptic activity in supraoptic neurons. The concentration of
the excitatory amino acid in the extracellular space was increased
pharmacologically by blocking glutamate transporters. Inhibition of the
astrocyte-specific GLT-1 glutamate transporter led to a reversible decrease in
evoked inhibitory postsynaptic current amplitude. This modulation had a
presynaptic origin as revealed by analysis of paired-pulse ratio and miniature
inhibitory currents. Furthermore, blocking group III metabotropic glutamate
receptors with the specific antagonist MAP4 prevented the depression of GABAergic
transmission induced by glutamate transporter blockade. Thus, presynaptic
metabotropic glutamate receptors located on inhibitory terminals in the
supraoptic nucleus appear to sense changes in ambient glutamate and modify GABA
release accordingly. However, it seems that such changes need to reach a certain
magnitude because the discrete deficit in glutamate clearance which occurs in the
supraoptic nucleus of lactating rats is not sufficient to modulate GABA-mediated
transmission. These results suggest that ambient glutamate contributes to the
modulation of synaptic efficacy not only at glutamatergic synapses but also at
inhibitory GABAergic synapses.

DOI: 10.1046/j.1460-9568.2003.02611.x
PMID: 12752776 [Indexed for MEDLINE]

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