Js. Isaacson et B. Walmsley, AMPLITUDE AND TIME-COURSE OF SPONTANEOUS AND EVOKED EXCITATORY POSTSYNAPTIC CURRENTS IN BUSHY CELLS OF THE ANTEROVENTRAL COCHLEAR NUCLEUS, Journal of neurophysiology, 76(3), 1996, pp. 1566-1571
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.