Abstract

It is commonly recognized that physical exercise positively affects several CNS regions and improves cognitive abilities. For example, exercise is associated with an increase in neurogenesis and facilitation of long-term potentiation in the hippocampus. Conversely, animal models for depression are associated with a decrease in neurogenesis and a reduction of long-term potentiation in the hippocampus. Although exercise could be a viable option in the treatment of some forms of depression, the mechanisms responsible for such improvements have not been elucidated. In this study, we examine hippocampal function using electrophysiological field recordings in CA1 and dentate gyrus to study baseline synaptic transmission and long-term potentiation in adolescent and adult rats prenatally exposed to the glucocorticoid dexamethasone. One group of animals was allowed to run voluntarily for 10 or 21 days using an exercise wheel before the experiments, and the control group was prevented from running (i.e. the exercise wheel was locked). In adult saline-exposed animals, exercise was associated with increased long-term potentiation in the dentate gyrus. Unexpectedly, in dexamethasone-exposed animals, dentate gyrus long-term potentiation was facilitated, whereas long-term potentiation in CA1 was unaffected by prenatal dexamethasone or by 10 or 21 days of voluntary running. Irrespective of age, prenatal dexamethasone and running had limited effects on synaptic transmission and presynaptic release in CA1 and dentate gyrus. In summary, running facilitates dentate gyrus long-term potentiation in adult animals that resembles the effects of prenatal dexamethasone.

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