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In experiments on rats was simulated the behavioral depression caused by social isolation and chronic inflammation. It was found in slices of the medial prefrontal cortex that behavioral depression was attained by the inhibition of the basal glutamatergic synaptic transmission in the layer V pyramidal neurons of the medial prefrontal cortex, that was manifested by decay of the amplitude of field (f) excitatory postsynaptic potentials (EPSPs). The increase of amlitude of N-methyl-D-aspartate (NMDA) component of fEPSPs in addition observed. Last effect was conditioned by the increase of the functional activity of the NMDA receptors (NMDARs) containing NR2A subunit. The increase of functional activity of the NMDARs evoked inhibition of the basal glutamatergic synaptic transmission in the pyramidal neurons, whereas it was prevented by systemic administration of NMDARs blocker ketamine. It was observed also under behavioral depression disturbances of the plastic properties of cortical synapses, which become apparent by the inhibition of the expression of long-term potentiation and long-term depression of synaptic transmission, but with the reinforcement of the last under the induced by social isolation of behavioral depression. The disturbances of synaptic plasticity are conditioned par excellence by increase of functional activity of verapamil-sensetive Ca 2+ channels.

The Glutamatergic Synaptic Transmission Mediated by Ionotropic Glutamate Receptors in Rats Cerebral Cortex in Behavioral Depression