Colloque

Nécessité des récepteurs GABAB pour la production de la PLT des réponses inhibitrices induites par une stimulation thêta dans la région CA1 de l'hippocampe

Andrew Chapman

Christian Patenaude

Jean-Claude Lacaille

Membre a labase

Andrew Chapman

Résumé du colloque

Long-term potentiation of excitatory synaptic responses in hippocampal CA1 pyramidal neurons is accompanied by changes in GABAergic inhibition mediated by local interneurons. Past work in our laboratory showed that polysynaptic IPSPs in pyramidal cells are potentiated to a greater extent when theta-burst stimulation (TBS) rather than 100 Hz tetani is used to induce LTP. To determine if the potentiation is due partly to direct strengthening of inhibitory synaptic transmission, we examined changes in pharmacologically isolated monosynaptic IPSPs in CA1 pyramidal cells following either TBS or 100 Hz tetanization. In experiments with sharp electrodes filled with 4M KAc and 0.01M KCl, 100 Hz tetanization caused only short-term (<5 min) depression of GABAA IPSPs with no lasting changes. In contrast, TBS induced a significant potentiation of IPSPs (114 ± 3 % of control) that peaked 5-10 min after stimulation and persisted for at least 20 min. Mechanisms underlying the potentiation were investigated using visually-guided whole-cell recordings with K-gluconate as the primary recording electrolyte. Monosynaptic IPSPs were significantly potentiated by TBS in these recordings. The potentiation was blocked by bath application of the GABAB receptor antagonist CPG55845A. Further, potentiation was blocked when postsynaptic G-protein activation was blocked with GDP- -s. This suggests that potentiation of monosynaptic IPSPs following TBS results from GABAB receptor-mediated activation of postsynaptic G-proteins. These results provide further support for the role of theta activity in synaptic plasticity, and suggest a role for GABAB receptors in plasticity of inhibitory synapses.