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The functional properties of spontaneous, glutamatergic EPSCs and non-NMDA receptors in AII amacrine cells were studied in whole cells and patches from slices of the rat retina using single and dual electrode voltage clamp recording. Pharmacological analysis verified that the EPSCs (Erev ~0 mV) were mediated exclusively by AMPA-type receptors. EPSCs displayed a wide range of waveforms, ranging from simple monophasic events to more complex multiphasic events. Amplitude distributions of EPSCs were moderately skewed towards larger amplitudes (modal peak 23 pA). Interevent interval histograms were best fitted with a double exponential function. Monophasic, monotonically rising EPSCs displayed very fast kinetics with an average 10-90 % rise time of ~340 µs and a decay phase well fitted by a single exponential (decay ~760 µs). The specific AMPA receptor modulator cyclothiazide markedly slowed the decay phase of spontaneous EPSCs (
decay ~3 ms). An increase in temperature decreased both 10-90 % rise time and
decay with Q10 values of 1.3 and 1.5, respectively. The decay kinetics were slower at positive membrane potentials compared to negative membrane potentials (205 mV/e-fold change in
decay). Step depolarization of individual presynaptic rod bipolar cells or OFF-cone bipolar cells evoked transient, CNQX-sensitive responses in AII amacrine cells with average peak amplitudes of ~330 pA. Ultrafast application of brief (~1 ms) or long (~500 ms) pulses of glutamate to outside-out patches evoked strongly desensitizing responses with very fast deactivation and desensitization kinetics, well fitted by single (
decay ~1.1 ms) and double exponential (
1 ~3.5 ms;
2 ~21 ms) functions, respectively. Double-pulse experiments indicated fast recovery from desensitization (
~12.4 ms). Our results indicate that spontaneous, AMPA receptor-mediated EPSCs in AII amacrine cells have very fast, voltage-dependent kinetics that can be well accounted for by the kinetic properties of the AMPA receptors themselves.
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