Abstract
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.
Highlights
According to NMR- and PET-spectroscopy patients with depressive disorders has higher local blood flow and elevation of glucose metabolism in certain limbic structures of a brain compared to nondepressed people (Mayberg et al, 1999 and Moore et al, 2009)
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 curves of dependence of the fEPSP amplitudes from intensity of presynaptic stimulation characterized by value of a slope of curve, which was determined from linear regression in the linear range of the input-output relationship estabilished by plotting the amplitude of fEPSPs in response to voltage pulse
Summary
According to NMR- and PET-spectroscopy patients with depressive disorders has higher local blood flow and elevation of glucose metabolism in certain limbic structures of a brain compared to nondepressed people (Mayberg et al, 1999 and Moore et al, 2009). Depressive state is generally associated with activation of the neuronal ensembles in dorsolateral prefrontal cortex, subgenual part of anterior cingulate cortex, amygdala, and ventrolateral thalamus (Price and Drevets, 2010). The projection neurons of these structures are glutamatergic. It is reasonable to suppose that one of the neurophysiological components of
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
