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Effects of adrenalectomy on Ca 2+ currents and Ca 2+ channel subunit mRNA expression in hippocampal CA1 neurons of young rats
Author(s) -
Karst H.,
Werkman T.R.,
Struik M.,
Bosma A.,
Joëls M.
Publication year - 1997
Publication title -
synapse
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.809
H-Index - 106
eISSN - 1098-2396
pISSN - 0887-4476
DOI - 10.1002/(sici)1098-2396(199706)26:2<155::aid-syn6>3.0.co;2-7
Subject(s) - hippocampal formation , endocrinology , medicine , adrenalectomy , chemistry , protein subunit , hippocampus , synapse , electrophysiology , ion channel , biophysics , neuroscience , biology , receptor , biochemistry , gene
Previously it was found that the amplitude of Ca currents in CA1 hippocampal neurons increases after adrenalectomy (ADX) of young adult rats. Preliminary data suggested that this effect of ADX is age‐dependent. In the present study we therefore investigated the effect of ADX on Ca currents in three age groups: rats that were 1, 3, or 6 months old. It appeared that ADX of the youngest age group resulted in a selective enhancement of sustained, high threshold Ca currents. By contrast, ADX of the oldest rats enhanced only the low threshold, transient Ca current amplitude. The age dependency of the ADX‐induced effects can be explained by developmental changes in Ca current properties in the adrenally intact rats with which ADX animals were compared. Data from acutely dissociated cells, which lack most of their dendrites, suggest that the ADX‐induced changes of Ca current properties are at least partly targeted at currents generated in the distal dendrites. No significant changes were observed with age or after ADX for the mRNA expression of the α1D Ca channel subunit, which forms the ionpore of the sustained high threshold L‐type Ca channel. We can therefore presently not exclude that the altered amplitude of Ca current with age and ADX is due to changes in ion channel function rather than in the total number of these channels. Synapse 26:155–164, 1997. © 1997 Wiley‐Liss, Inc.