Abstract
Whole cell patch clamp recording, Ca2+ measurement with ratiometric fluorescent dyes and photolysis of caged Ca2+ were combined to investigate the depolarization- and photolysis-induced suppression of inhibition (DSI and PSI) in rat hippocampal CA1 pyramidal cells. A 5-s depolarization from −70 mV to 0 mV or a 6-s photolysis of nitrophenyl-EGTA (NPE) in cell bodies could each depress the frequency of spontaneous inhibitory postsynaptic currents (IPSCs) and the amplitude of evoked IPSCs while elevating intracellular Ca2+ concentration ([Ca2+]i). Within a cell the elevation of [Ca2+]i induced by depolarization was inversely related to that induced by photolysis, suggesting that higher [NPE] is more effective in releasing caged Ca2+ but also increases buffer capacity to reduce [Ca2+]i rises caused by Ca2+ influx through voltage-dependent Ca2+ channels. Both DSI and PSI were linearly related to [Ca2+]i, with a 50 % reduction in transmission occurring at about 3.6–3.9 μM. [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. We conclude that DSI is activated by micromolar [Ca2+]i acting far from sites of Ca2+ entry through channels in the plasma membrane.