NDLI: N- and L-type calcium channel involvement in depolarization-induced suppression of inhibition in rat hippocampal CA1 cells

Content Provider	PubMed Central
Author	Lenz, R. A. Wagner, J. J. Alger, B. E.
Copyright Year	1998
Abstract	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 GABAAergic IPSCs lasting for ∼1 min, was induced by depolarizing the pyramidal cell to −10 or 0 mV for 1 or 2 s. Raising extracellular Ca2+ concentration increased DSI, and varying the DSI-inducing voltage step showed that the voltage dependence of DSI was like that of high-voltage-activated Ca2+ channels. The P- and Q-type Ca2+ channel blocker ω-agatoxin TK (200 nm and 1 μm) and the R- and T-type Ca2+ channel blocker Ni2+ (100 μm) reduced IPSCs without reducing DSI. The specific N-type Ca2+ channel antagonist ω-conotoxin GVIA (250 nm) reduced IPSC amplitudes and almost completely abolished DSI. Blocking L-type Ca2+ channels with nifedipine (10 μm) had no effect on IPSCs or DSI induced by our standard protocol, but reduced DSI induced by the unclamped Na+- and Ca2+-dependent spikes that occurred when 2(triethylamino)-N-(2,6-dimethylphenyl)acetamide (QX-314) was omitted from the recording pipette solution. Although intracellular Ca2+ stores were not measured, DSI was not affected by cyclopiazonic acid (CPA, 20–40 μm), a blocker of Ca2+ uptake into intracellular stores. We conclude that DSI is initiated by Ca2+ influx through N- and, under certain conditions, L-type Ca2+ channels.
Related Links	http://dx.doi.org/10.1111/j.1469-7793.1998.061bf.x
Ending Page	73
Page Count	13
Starting Page	61
File Format	PDF
ISSN	00223751
e-ISSN	14697793
Journal	The Journal of Physiology
Issue Number	Pt 1
Volume Number	512
Language	English
Publisher	Blackwell Science Inc
Publisher Date	1998-10-01
Access Restriction	Open
Rights Holder	Blackwell Science Inc
Subject Keyword	Physiology Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Physiology Sports Science

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