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Calcium‐dependent inactivation of high‐threshold calcium currents in human dentate gyrus granule cells
Author(s) -
Nägerl U. Valentin,
Mody Istvan
Publication year - 1998
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1111/j.1469-7793.1998.039bo.x
Subject(s) - dentate gyrus , calcium , granule (geology) , biophysics , chemistry , neuroscience , biology , hippocampal formation , paleontology , organic chemistry
1 Dentate gyrus granule cells acutely dissociated from hippocampal slices obtained from chronic temporal lobe epilepsy (TLE) patients displayed a high‐voltage activated (HVA) Ca 2+ conductance with a pronounced Ca 2+ ‐dependent inactivation. 2 Inactivation time constants and peak HVA Ca 2+ current ( I Ca ) amplitudes did not differ between perforated patch and whole‐cell recordings without added exogenous Ca 2+ buffers, indicating that the Ca 2+ ‐dependent characteristics of I Ca inactivation were well preserved in whole‐cell recordings. 3 Inactivation time constants correlated with whole‐cell I Ca , and were increased when Ca 2+ was replaced with Ba 2+ in the external solution or 5 m m BAPTA was added to the pipette solution. 4 In recordings without added exogenous Ca 2+ buffers, the time course of I Ca inactivation was comparable between human TLE and kindled rat granule cells. Conversely, the time course of I Ca in human TLE granule cells loaded with 5 m m intracellular BAPTA resembled that observed in buffer‐free recordings from control rat neurones. 5 The loss of a putative intraneuronal Ca 2+ buffer, the Ca 2+ ‐binding protein calbindin (CB), from human granule cells during TLE may result in the pronounced Ca 2+ ‐dependent I Ca inactivation. This process could serve a neuroprotective role by significantly decreasing Ca 2+ entry during prolonged trains of action potentials known to occur during seizures.