AMPLITUDE AND TIME-COURSE OF SPONTANEOUS AND EVOKED EXCITATORY POSTSYNAPTIC CURRENTS IN BUSHY CELLS OF THE ANTEROVENTRAL COCHLEAR NUCLEUS

1. Spontaneous and evoked excitatory postsynaptic currents (EPSCs) wer e recorded in slices of the rat anteroventral cochlear nucleus (AVCN) at the endbulb-bushy cell synaptic connection. 2. The amplitudes of lp ha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA)-receptor- mediated spontaneous EPSCs were large (54 +/- 6 pA, mean +/- SD; membr ane potential = -70 mV, 22-25 degrees C) and, in the same cell, exhibi ted a very wide range of peak amplitudes (CV = 0.42 +/- 0.01, n = 15 c ells). There was no significant correlation between rise times or deca y time constants and the peak amplitudes of spontaneous EPSCs recorded in the same cell, demonstrating that electrotonic attenuation is not responsible for the large amplitude variability of spontaneous EPSCs. 3. Cyclothiazide, a potent blocker of AMPA-receptor desensitization, d id not affect the amplitude of spontaneous EPSCs in AVCN bushy cells, suggesting that background desensitization of AMPA receptors is not si gnificant in these cells. However, the decay time constant of spontane ous EPSCs was prolonged significantly (2.6-fold increase). In addition , cyclothiazide produced a marked increase (similar to 40%, n = 6 cell s) in the frequency of spontaneous EPSCs, indicating a likely presynap tic site of action of this drug. 4. Cyclothiazide produced a small inc rease (similar to 10%, n = 7 cells) in the peak amplitude of the evoke d endbulb EPSC, but this effect could be explained by the action of cy clothiazide to increase the decay time constant of the underlying quan tal EPSCs in conjunction with the asynchrony of quantal transmitter re lease at the endbulb synapse. 5. These results indicate that neither e lectrotonic attenuation nor receptor desensitization are responsible f or the wide range of peak amplitudes of spontaneous EPSCs in bushy cel ls. The large quantal variability therefore is likely to be due entire ly to intrinsic fluctuations at each release site and site-to-site var iability in the numbers of available receptors.