RESUMO
AIM: To study an effect of corticosterone (100 nM) on spontaneous inhibitory postsynaptic currents (sIPSC) in pyramidal neurons of CA1 area and a role of inhibitory CB1-expressing synapses in the development of corticosterone-induced effects. MATERIAL AND METHODS: The experiments were performed on acute slices of the rat ventral hippocampus using whole-cell configuration of the patch-clamp technique. RESULTS AND CONCLUSION: The addition of corticosterone resulted in a small, but significant, increase in the frequency of sIPSCs during the first 10 minutes and then this parameter returned to the basal level. Corticosterone treatment resulted in a considerable decrease in the sIPSC amplitude 40 minutes after the beginning of treatment. The activation of CB1 receptors weakly affected sIPSC characteristics, however, the addition of corticosterone did not induce the rapid elevation in the sIPSC frequency, which occurred on the 10th minute in the control, as well as a decrease in the sIPSC amplitude, which was observed in the control on the 40th min after the beginning of corticosterone treatment. The data obtained suggest that both rapid and slow effects of corticosterone are associated with the activity of CB1-expressing inhibitory synapses of the hippocampus.
Assuntos
Região CA1 Hipocampal/efeitos dos fármacos , Corticosterona/farmacologia , Potenciais Pós-Sinápticos Inibidores/efeitos dos fármacos , Células Piramidais/efeitos dos fármacos , Receptor CB1 de Canabinoide/metabolismo , Sinapses/efeitos dos fármacos , Transmissão Sináptica/efeitos dos fármacos , Animais , Região CA1 Hipocampal/metabolismo , Região CA1 Hipocampal/fisiopatologia , Técnicas de Patch-Clamp , Ratos , Ratos WistarRESUMO
Experiments were performed on cultured slices of rat ventral hippocampus. Using extracellular stimulation and patch clamp recording from pyramidal neurons in the hippocampal CA1 area, we studied characteristics of GABAergic synapse formed on these neurons by cholecystokinin-expressing interneurons. This synapse was characterized by asynchronous release of GABA and depolarization-induced suppression of inhibitory response. It was observed that administration of corticosterone increased the amplitude of evoked inhibitory postsynaptic currents in 5 minutes, but the paired ratio did not significantly change. Obtained data reflect that corticosterone can induce rapid genome-independent effects on inhibitory neurotransmission in one of hippocampal synapses.