1. Whole cell patch clamp recording, Ca2+ measurement with ratiometric fluo
rescent dyes and photolysis of caged Ca2+ were combined to investigate the
depolarization- and photolysis-induced suppression of inhibition (DSI and P
SI) in rat hippocampal CA1 pyramidal cells.
2. A 5-s depolarization from -70 mV to 0 mV or a 6-s photolysis of nitrophe
nyl-EGTA (NPE) in cell bodies could each depress the frequency of spontaneo
us inhibitory postsynaptic currents (IPSCs) and the amplitude of evoked IPS
Cs while elevating intracellular Ca2+ concentration ([Ca2+](i)).
3. Within a cell the elevation of [Ca2+](i) induced by depolarization was i
nversely related to that induced by photolysis, suggesting that higher [NPE
] is more effective in releasing caged Ca2+ hut also increases buffer capac
ity to reduce [Ca2+](i) rises caused by Ca2+ influx through voltage-depende
nt Ca2+ channels.
4. Both DSI and PSI were linearly related to [Ca2+](i), with a 50 % reducti
on in transmission occurring at about 3.6-3.9 muM.
5. [Ca2+](i) recovered more quickly than DSI, indicating that the duration
of DSI is not set simply by the duration of [Ca2+](i) elevation, but rather
entails other rate-limiting processes.
6. We conclude that DSI is activated by micromolar [Ca2+](i) acting far fro
m sites of Ca2+ entry through channels in the plasma membrane.