1 The effect of a low concentration (1 μM) of kainate (kainic acid; KA) on presynaptic calcium (Ca2+) influx at the Schaffer collateral‐commissural (SCC) synapse was examined in rat hippocampal slices. 2 Following selective loading of the presynaptic terminals with the fluorescent Ca2+ indicator rhod‐2 AM, transient increases in the presynaptic Ca2+ concentration (pre(Ca2+)t) and field excitatory postsynaptic potentials (EPSPs) evoked by electrical stimulation of the SCC pathway were recorded simultaneously. 3 Bath application of 1 μM KA reversibly suppressed field EPSPs and pre(Ca2+)t to 37.7 ± 4.0 % and 72.9 ± 2.4 % of control, respectively. Excitatory postsynaptic currents (EPSCs) recorded with the use of the whole‐cell patch‐clamp technique were also suppressed by 1 μM KA to 42.6 ± 6.3 % of control. A quantitative analysis of the decreases in pre(Ca2+)t and the amplitude of field EPSP during KA application suggests that KA inhibits transmission primarily by reducing the pre(Ca2+)t. 4 Consistent with a presynaptic site for these effects, paired‐pulse facilitation (PPF) was enhanced by 1 μM KA. 5 A substantial KA‐induced suppression of NMDA receptor‐mediated EPSPs was detected when AMPA receptors were blocked by the AMPA receptor‐selective antagonist GYKI 52466 (100 μM). 6 The suppressive effect of KA on field EPSPs and pre(Ca2+)t was antagonized by the KA antagonist NS‐102 (10 μM). 7 These results suggest that the presynaptic inhibitory action of KA at the hippocampal CA1 synapse is primarily due to the inhibition of Ca2+ influx into the presynaptic terminals.
The Journal of Physiology – Wiley
Published: Jun 1, 1998
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