EN
Chronic stress and elevated level of corticosterone have been implicated in a variety of pathophysiological processes including mood disorders. A growing body of evidence links cognitive dysfunctions with abnormalities of excitatory transmission in the brain. We studied glutamatergic transmission and synaptic plasticity in the frontal cortex after exposure of rats to two different types of stress: crowding and restraint. Additionally, repeated corticosterone administration was employed as a model of non-adaptive stress. Electrophysiological experiments were performed on ex vivo frontal cortical slices prepared 24 h after last stress session. In slices originating from stressed and corticosterone-treated animals the amplitude of extracellular field potentials recorded in cortical layer II/III was increased and the magnitude of long-term potentiation (LTP) was decreased. Whole-cell recoding from layer II/III pyramidal neurons demonstrated corticosterone treatment-induced increase in the frequency of spontaneous excitatory postsynaptic currents (sEPSCs). These data point to an enhancement of excitatory transmission in the frontal cortex resulting from an increased glutamate release as a common effect of different types of stress. Support: grant POIG 01.01.02-12-004/09-00 from the European Regional Development Fund