Ra. Lenz et al., N-TYPE AND L-TYPE CALCIUM-CHANNEL INVOLVEMENT IN DEPOLARIZATION-INDUCED SUPPRESSION OF INHIBITION IN RAT HIPPOCAMPAL CA1 CELLS, Journal of physiology, 512(1), 1998, pp. 61-73
1. We investigated depolarization-induced suppression of inhibition (D
SI) under whole-cell voltage clamp in CA1 pyramidal neurons of rat hip
pocampal slices. DSI, a transient reduction in monosynaptic evoked GAB
A(A)ergic IPSCs lasting for similar to 1 min, was induced by depolariz
ing the pyramidal cell to -10 or 0 mV for 1 or 2 s. 2. Raising extrace
llular Ca2+ concentration increased DSI, and varying the DSI-inducing
voltage step showed that the voltage dependence of DSI was like that o
f high-voltage-activated Ca2+ channels. 3. The P- and Q-type Ca2+ chan
nel blocker omega-agatoxin TK (200 nM and 1 mu M) and the R- and T-typ
e Ca2+ channel blocker Ni2+ (100 mu M) reduced IPSCs without reducing
DSI. 4. The specific N-type Ca2+ channel antagonist omega-conotoxin GV
IA (250 nM) reduced IPSC amplitudes and almost completely abolished DS
I. 5. Blocking L-type Ca2+ channels with nifedipine (10 mu M) had no e
ffect on IPSCs or DSI: induced by our standard protocol, but reduced D
SI induced by the unclamped Na+- and Ca2+ dependent spikes that occurr
ed when 2(triethylamino) -N-(2,6 -dimethylphenyl)acetamide (QX-314) wa
s omitted from the recording pipette solution. 6. Although intracellul
ar Ca2+ stores were not measured, DSI was not affected by cyclopiazoni
c acid (CPA, 20-40 mu M), 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.