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J Neurophysiol 95: 428-452, 2006. First published September 21, 2005; doi:10.1152/jn.00447.2005
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Transmission Between Type II Hair Cells and Bouton Afferents in the Turtle Posterior Crista

Joseph C. Holt, Jin-Tang Xue, Alan M. Brichta and Jay M. Goldberg

Department of Neurobiology, Pharmacology and Physiology, University of Chicago, Chicago Illinois

Submitted 2 May 2005; accepted in final form 12 September 2005

Synaptic activity was recorded with sharp microelectrodes during rest and during 0.3-Hz sinusoidal stimulation from bouton afferents identified by their efferent-mediated inhibitory responses. A glutamate antagonist, 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) decreased quantal size (qsize) while lowering external Ca2+ decreased quantal rate (qrate). Miniature excitatory postsynaptic potentials (mEPSPs) had effective durations (qdur) of 3.5–5 ms. Their timing was consistent with Poisson statistics. Mean qsizes ranged in different units from 0.25 to 0.73 mV and mean qrates from 200 to 1,500/s; there was an inverse relation across the afferent population between qrate and qsize. qsize distributions were consistent with the independent release of variable-sized quanta. Channel noise, measured during AMPA-induced depolarizations, was small compared with quantal noise. Excitatory responses were larger than inhibitory responses. Peak qrates, which could approach 3,000/s, led peak excitatory mechanical stimulation by 40°. Quantal parameters varied with stimulation phase with qdur and qsize being maximal during inhibitory stimulation. Voltage modulation (vmod) was in phase with qrate and had a peak depolarization of 1.5–3 mV. On average, 80% of vmod was accounted for by quantal activity; the remaining 20% was a nonquantal component that persisted in the absence of quantal activity. The extracellular accumulation of glutamate and K+ are potential sources of nonquantal transmission and may provide a basis for the inverse relation between qrate and qsize. Comparison of the phases of synaptic and spike activity suggests that both presynaptic and postsynaptic mechanisms contribute to variations across afferents in the timing of spikes during sinusoidal stimulation.


Address for reprint requests and other correspondence: J. M. Goldberg, Dept. of Neurobiology, Pharmacology, and Physiology, Univ. of Chicago, 947 E. 58th St., MC 0926, Chicago IL 60637 (E-mail: jgoldber{at}bsd.uchicago.edu)




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