Abstract

Rats were submitted to forced swimming and were killed 15 min after initiation of the stress and at 1 h, 1 day and 4 days thereafter. Immediately after the stress there was a decrease of 30% in the density of [3H]flunitrazepam binding sites in the cerebral cortex and of 27% in the hippocampal formation, with no changes in all the other brain areas studied. These changes in the number of benzodiazepine receptors were also corroborated by the binding of [3H]ethyl-beta-carboline carboxylate. For both ligands there were no changes in affinity. These effects were selective for the benzodiazepine receptors and no changes in alpha 1, alpha 2 and beta adrenoceptors and in dopaminergic receptors were observed. One hour after the stress, the number of benzodiazepine receptors had recovered in the cerebral cortex (8% above the control) and had increased greatly in the hippocampal formation (+53%). One day after the stress, the [3H]flunitrazepam binding in the cerebral cortex reached the normal level but it was still slightly elevated (+16%) in the hippocampus. These results are discussed in relation to some contradictory findings in the literature and to the fact that the hippocampal formation is related to neural mechanisms underlying behavior and neuroendocrine regulation.