The alterations of neurophysiological parameters of the anterior cingulate cortex in the experimental depressive syndrome of different genesis

The rostral anterior cingulate cortex (ACC) is important unit of the brain default mode network. An operation of this network is overset in depressive disorders of different genesis. A hyperactivity of ACC marks this overset. Neurophysiological nature of ACC hyperactivity do not elucidate. It was reproduced a behavioral depression in experiments on the rats evoke by either chronic inflammation of back skin or depletion of level of the monoamines in the brain administration of reserpine. The level of rat depression behavior estimated on the data of scores of forced swimming test. It was ascertained in electrophysi-ological researches on brain slices comprising ACC that depressogenic procedures evoked appearance of pathological synaptic plasticity (analog of the long-term potentiation) in superficial II/III layers pyramidal neurons. This pathological plasticity appeared by increasing of the amplitudes of field EPSPs and their AMPA and NMDA components; it was due by gain of the presynaptic glutamate releasing and possible rising of the postsynaptic receptors chemosensitivity. Pathological synaptic plasticity occluded tetanus-induced longterm potentiation in these layers of ACC. The neurophysiological changes in deep V layer of ACC were inconsiderable, however it was ascertained inhibition of tetanus-induced long-term potentiation expression.

anterior cingulate cortex, layers, synaptic transmission, long-term potentiation, depressive syndrome, chronic inflammation, reserpine