Psychiatrists and Psychologists

It has been suggested that the neurons of prefrontal cortex, along with the hippocampus and amygdala, can undergoes morphological and molecular remodelling during the development of stress-related disorders, such as PTSD[1]. Pathological remodeling of the GABAergic inhibitory signalling during stress disorders might bring significant contribution to impairment of synaptic plasticity [2] and cognition [3]. In this work we have used an experimental model of PTSD in mice, based on a single prolonged stress protocol [4] and studied alterations in the synaptic transmission and long-term synaptic plasticity in the pyramidal neurons of prefrontal cortex.The stress state in the animals was evaluated with the aid of Open field and Elevated cross-maze behavioural tests. We have found an increase in the quantal amplitude of GABA-ergic spontenous inhibitory synaptic currents (mIPSCs) in the neurons of prefrontal cortex of stressed animals. There were also elevation in the frequency of mIPSC in neurons of the stress-group vs control group. These results demonstrate that that exposure to stress can cause an up-regulation of the GABAergic inhibitory system in the prefrontal cortex. In the experiments on long-term potatiation (LTP) of field postsynaptic potentials (fEPSP), we have observed that the amplitude of LTP induced by the theta-burst stimulation in the prefrontal cortex synapses of stressed mice was much lower than in the control group. The data obtained suggest that stress-induced up-regulation of inhibitory signalling can affect long-term synaptic plasticity in the prefrontal cortex and thereby contribute to congnitive impairment.