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Calcium store depletion induces persistent perisomatic increases in the functional density of h channels in hippocampal pyramidal neurons.


ABSTRACT: The regulation of intracellular calcium by the endoplasmic reticulum (ER) plays a critical role in neuronal function. While the consequences associated with depleting calcium from the ER have been studied in multiple systems, it is not known whether the intrinsic properties of a neuron change in response to such perturbations. In this study, we demonstrate that the depletion of calcium from the ER of hippocampal CA1 pyramidal neurons induces a persistent, perisomatic increase in the density of functional h channels resulting in a reduction in intrinsic excitability and an increase in the optimal response frequency. This form of intrinsic plasticity is dependent on the elevation of cytoplasmic calcium, inositol triphosphate receptors, store-operated calcium channels, and the protein kinase A pathway. We postulate that this form of depletion-induced intrinsic plasticity is a neuroprotective mechanism that reduces excitability after depletion of calcium stores triggered through altered network activity during pathological conditions.

SUBMITTER: Narayanan R 

PROVIDER: S-EPMC3024579 | biostudies-literature | 2010 Dec

REPOSITORIES: biostudies-literature

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Calcium store depletion induces persistent perisomatic increases in the functional density of h channels in hippocampal pyramidal neurons.

Narayanan Rishikesh R   Dougherty Kevin J KJ   Johnston Daniel D  

Neuron 20101201 5


The regulation of intracellular calcium by the endoplasmic reticulum (ER) plays a critical role in neuronal function. While the consequences associated with depleting calcium from the ER have been studied in multiple systems, it is not known whether the intrinsic properties of a neuron change in response to such perturbations. In this study, we demonstrate that the depletion of calcium from the ER of hippocampal CA1 pyramidal neurons induces a persistent, perisomatic increase in the density of f  ...[more]

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