Delayed effects of corticosterone on slow after-hyperpolarization potentials in mouse hippocampal versus prefrontal cortical pyramidal neurons.

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 (sAH...

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Main Authors: Anup G Pillai, Marloes J A G Henckens, Guillén Fernández, Marian Joëls
Format: Article
Language:English
Published: Public Library of Science (PLoS) 2014-01-01
Series:PLoS ONE
Online Access:http://europepmc.org/articles/PMC4047100?pdf=render
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author Anup G Pillai
Marloes J A G Henckens
Guillén Fernández
Marian Joëls
author_facet Anup G Pillai
Marloes J A G Henckens
Guillén Fernández
Marian Joëls
author_sort Anup G Pillai
collection DOAJ
description 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.
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spelling doaj.art-18ff45e66e09403ab9c03be79cf09c1b2022-12-22T03:17:42ZengPublic Library of Science (PLoS)PLoS ONE1932-62032014-01-0196e9920810.1371/journal.pone.0099208Delayed effects of corticosterone on slow after-hyperpolarization potentials in mouse hippocampal versus prefrontal cortical pyramidal neurons.Anup G PillaiMarloes J A G HenckensGuillén FernándezMarian JoëlsThe 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.http://europepmc.org/articles/PMC4047100?pdf=render
spellingShingle Anup G Pillai
Marloes J A G Henckens
Guillén Fernández
Marian Joëls
Delayed effects of corticosterone on slow after-hyperpolarization potentials in mouse hippocampal versus prefrontal cortical pyramidal neurons.
PLoS ONE
title Delayed effects of corticosterone on slow after-hyperpolarization potentials in mouse hippocampal versus prefrontal cortical pyramidal neurons.
title_full Delayed effects of corticosterone on slow after-hyperpolarization potentials in mouse hippocampal versus prefrontal cortical pyramidal neurons.
title_fullStr Delayed effects of corticosterone on slow after-hyperpolarization potentials in mouse hippocampal versus prefrontal cortical pyramidal neurons.
title_full_unstemmed Delayed effects of corticosterone on slow after-hyperpolarization potentials in mouse hippocampal versus prefrontal cortical pyramidal neurons.
title_short Delayed effects of corticosterone on slow after-hyperpolarization potentials in mouse hippocampal versus prefrontal cortical pyramidal neurons.
title_sort delayed effects of corticosterone on slow after hyperpolarization potentials in mouse hippocampal versus prefrontal cortical pyramidal neurons
url http://europepmc.org/articles/PMC4047100?pdf=render
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AT marianjoels delayedeffectsofcorticosteroneonslowafterhyperpolarizationpotentialsinmousehippocampalversusprefrontalcorticalpyramidalneurons