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

R. A. Lenz, J. J. Wagner and B. E. Alger

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_Aergic 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 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.

3. The P- and Q-type Ca²⁺ channel blocker -agatoxin TK (200 nM and 1 µM) and the R- and T-type Ca²⁺ channel blocker Ni²⁺ (100 µM) reduced IPSCs without reducing DSI.

4. The specific N-type Ca²⁺ channel antagonist -conotoxin GVIA (250 nM) reduced IPSC amplitudes and almost completely abolished DSI.

5. 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.

6. 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.

7. We conclude that DSI is initiated by Ca²⁺ influx through N- and, under certain conditions, L-type Ca²⁺ channels.