Premium
N‐ and L‐type calcium channel involvement in depolarization‐induced suppression of inhibition in rat hippocampal CA1 cells
Author(s) -
Lenz R. A.,
Wagner J. J.,
Alger B. E.
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.1469-7793.1998.061bf.x
Subject(s) - depolarization , chemistry , cyclopiazonic acid , channel blocker , biophysics , nifedipine , voltage dependent calcium channel , patch clamp , hippocampal formation , t type calcium channel , antagonist , calcium , intracellular , endocrinology , biochemistry , biology , receptor , organic chemistry
1 We investigated depolarization‐induced suppression of inhibition (DSI) under whole‐cell voltage clamp in CA1 pyramidal neurons of rat hippocampal slices. DSI, a transient reduction in monosynaptic evoked GABA A ergic IPSCs lasting for ∼1 min, was induced by depolarizing the pyramidal cell to −10 or 0 mV for 1 or 2 s. 2 Raising extracellular Ca 2+ concentration increased DSI, and varying the DSI‐inducing voltage step showed that the voltage dependence of DSI was like that of high‐voltage‐activated Ca 2+ channels. 3 The P‐ and Q‐type Ca 2+ channel blocker ω‐agatoxin TK (200 n m and 1 μ m ) and the R‐ and T‐type Ca 2+ channel blocker Ni 2+ (100 μ m ) reduced IPSCs without reducing DSI. 4 The specific N‐type Ca 2+ channel antagonist ω‐conotoxin GVIA (250 n m ) reduced IPSC amplitudes and almost completely abolished DSI. 5 Blocking L‐type Ca 2+ channels with nifedipine (10 μ m ) had no effect on IPSCs or DSI induced by our standard protocol, but reduced DSI induced by the unclamped Na + ‐ and Ca 2+ ‐dependent spikes that occurred when 2(triethylamino)‐ N‐ (2,6‐dimethylphenyl)acetamide (QX‐314) was omitted from the recording pipette solution. 6 Although intracellular Ca 2+ stores were not measured, DSI was not affected by cyclopiazonic acid (CPA, 20–40 μ m ), a blocker of Ca 2+ uptake into intracellular stores. 7 We conclude that DSI is initiated by Ca 2+ influx through N‐ and, under certain conditions, L‐type Ca 2+ channels.