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BACKGROUND AND AIMS: The hypothalamic paraventricular nucleus (PVN) plays a key role in the activation of the hypothalamic-pituitary-adrenal axis (HPA). In response to stress, corticotropin releasing hormone (CRH) is released from parvocellular PVN neurosecretory neurons into hypophysial portal vessels that access the anterior pituitary gland to stimulate the production of the adrenocorticotropic hormone (ACTH), which stimulates the adrenal cortex to produce glucocorticoid hormones. It is known that excitatory and inhibitory inputs that regulate the activity of parvocellular PVN neurosecretory neurons may undergo stress-related modifications. However, the influence of acute restraint stress on the function of glutamatergic and GABAergic synapses in PVN is not fully understood. METHODS: Adolescent male Wistar rats were subjected to acute restraint lasting 10 min. Animals were decapitated either immediately after the stress session or 24 hours later. Whole-cell patchclamp was used to record spontaneous and miniature excitatory and inhibitory postsynaptic currents (sEPSCs/mEPSCs, sIPSCs/ mIPSCs) from parvocellular neuroendocrine neurons of the PVN ex vivo. RESULTS: In animals decapitated immediately after the stress session, an increase in the mean frequency of sEPSCs/mEPSCs was observed. These effects were accompanied by a decrease in the mean frequency of sIPSCs/mIPSCs. The kinetics and amplitude of the currents remained unchanged. In slices prepared 24 h after the restraint there was no change in the frequency and amplitude of all recorded currents. Also the basal electrophysiological properties and the excitability of the neurosecretory parvocellular neurons remained unchanged in all tested slices. CONCLUSIONS: Acute immobilization stress results in a transient (less than 24 h) enhancement of the glutamatergic and an attenuation of the GABAergic synaptic input to neurosecretory parvocellular neurons in the rat PVN. Support: Grant 2012/07/N/NZ4/02687.