Abstract

Long-term potentiation of excitatory synaptic transmission was studied in an in vitro turtle brain that manifests spontaneous electrocorticogram activity. We show that in the turtle medial cortex, there is evidence of homosynaptic long-term potentiation in the septum–medial cortex pathway. This potentiation has two components, one dependent on NMDA receptor activation and the other independent of this receptor and suppressed by nifedipine, an antagonist of voltage-dependent Ca 2+ channels (VDCCs), as occurs in the CA1 of rat hippocampus. Heterosynaptic long-term potentiation was also found in the medial cortex, as a tetanus in the septum also increased the cortico medial–cortico medial response. The intracellular response of pyramidal cells showed that the medial cortex EPSP increased its amplitude paripassu with an increase in the response of evoked field potential after tetanic stimulation in the septum.

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