Effects of repeated corticosterone administartion on synaptic transmission and plasticity in rat frontal cortex
Alterations in the functions of glutamatergic and GABAergic systems, as well as disturbances in synaptic plasticity related to cognitive functions have been linked to the patophysiology of mood disorders. High level of glucocorticoids in the circulatory system observed after prolonged exposure to stress is considered as major cause of depression. Repeated corticosterone administration represents an animal model to study the effects of non-adaptative stress. The aim of the present study was to examine the influence of repeated corticosterone administration on excitatory and inhibitory synaptic transmission as well as long-term potentiation (LTP) in ex vivo slices of the frontal cortex. Male Wistar rats were treated with corticosterone (10 mg/kg s.c.; suspended in 1% Tween 80) twice daily, for 7 or 21 days. Frontal cortical slices were prepared 48 hours after last drug administration. Whole-cell recordings of spontaneous excitatory postsynaptic currents (sEPSCs) and spontaneous inhibitory postsynaptic currents (sIPSCs) were made from layer II/III pyramidal cells at the holding membrane potential of -78 mV and 0 mV, respectively. Extracellular recordings of field potentials evoked by stimulation of layer V were made from layer II/III. We observed an increase of the mean sEPSCs frequency in slices prepared from animals treated with corticosterone for 7 and 21 days while the mean sEPSCs amplitude remained unchanged. In contrast, no corticosterone-induced changes in parameters characterizing sIPSCs were evident. After 7 and 21 days of stress hormone administration LTP was reduced. These data demonstrate that repeated corticosterone treatment enhances basal glutamatergic transmission and concurrently attenuates LTP. In contrast, GABAergic transmission remained unaffected by corticosterone.
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