Abstract
The rodent stress hormone corticosterone changes neuronal activity in a slow and persistent manner through transcriptional regulation. In the rat dorsal hippocampus, corticosterone enhances the amplitude of calcium-dependent potassium currents that cause a lingering slow after-hyperpolarization (sAHP) at the end of depolarizing events. In this study we compared the putative region-dependency of the delayed effects of corticosterone (approximately 5 hrs after treatment) on sAHP as well as other active and passive properties of layer 2/3 pyramidal neurons from three prefrontal areas, i.e. the lateral orbitofrontal, prelimbic and infralimbic cortex, with the hippocampus of adult mice. In agreement with previous studies, corticosterone increased sAHP amplitude in the dorsal hippocampus with depolarizing steps of increasing amplitude. However, in the lateral orbitofrontal, prelimbic and infralimbic cortices we did not observe any modifications of sAHP amplitude after corticosterone treatment. Properties of single action potentials or % ratio of the last spike interval with respect to the first spike interval, an indicator of accommodation in an action potential train, were not significantly affected by corticosterone in all brain regions examined. Lastly, corticosterone treatment did not induce any lasting changes in passive membrane properties of hippocampal or cortical neurons. Overall, the data indicate that corticosterone slowly and very persistently increases the sAHP amplitude in hippocampal pyramidal neurons, while this is not the case in the cortical regions examined. This implies that changes in excitability across brain regions reached by corticosterone may vary over a prolonged period of time after stress.
Highlights
Exposure of an organism to stressful conditions causes the adrenal glands to release high amounts of corticosteroids
Two types of receptors have been identified: the mineralocorticoid receptor (MR), which due to its high affinity for corticosterone is already substantially activated under rest; and the lower-affinity glucocorticoid receptor (GR), which is occupied after stress [2]
Despite the fact that GRs are rather ubiquitous in the brain, their role in modulating neuronal excitability has so far mostly been studied in the dorsal hippocampus
Summary
Exposure of an organism to stressful conditions causes the adrenal glands to release high amounts of corticosteroids (cortisol in primates, corticosterone in rats and mice). Downstream of the calcium influx, activation of calcium-dependent potassium channels may occur, in particular currents involved in the accommodation of firing frequency during periods of depolarization and the lingering slow after-hyperpolarization (sAHP) when the depolarization is terminated [10] In line with this cascade, several studies have demonstrated that 1–4 hrs after administration of a brief pulse of corticosterone to pyramidal neurons in the rat dorsal CA1 hippocampal area, the amplitude of the sAHP is enhanced [11,12,13]; effects on firing frequency were somewhat more ambiguous [11,13]. The alterations in sAHP amplitude by corticosterone in the aftermath of stress might be a crucial mechanism for normalizing the rapid increases of excitability observed soon after stress onset [17]
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