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J Neurophysiol (February 28, 2007). doi:10.1152/jn.01148.2006
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Submitted on October 29, 2006
Accepted on February 23, 2007

Electrically-Evoked Responses in Onset Chopper Neurons in Guinea Pig Cochlear Nucleus

Wilhelmina H Mulders1, Alan Robert Harvey2, and Donald Robertson3*

1 Physiology, School of Biomedical, Biomolecular and Chemical Sciences, University of Western Australia, Crawley, Western Australia, Australia
2 School of Anatomy and Human Biology, University of western Australia, Crawley, Western Australia, Australia
3 Physiology, University of Western Australia, 6009 Nedlands, Australia; Physiology, School of Biomedical, Biomolecular and Chemical Sciences, University of Western Australia, Crawley, Western Australia, Australia; Physiology, University of Western Australia, Crawley, Western Australia, Australia

* To whom correspondence should be addressed. E-mail: drobed{at}cyllene.uwa.edu.au.

Extracellular recordings were obtained from single cochlear nucleus neurons in guinea pigs anaesthetized with Nembutal and Hypnorm. Neurons were classified by their spontaneous firing rates and responses to acoustic stimuli. In addition, electrical shocks were applied to the midline at the level of the IVth ventricle and spike responses were recorded. Spikes were only evoked by shocks in neurons that were classified as onset choppers (Oc). The shock-evoked spikes could be extinguished by acoustically-evoked action potentials in the same neurons. In about 30% of the sample of Oc neurons, quantitative aspects of the timing of this extinction were not compatible with the shock-evoked spike being antidromically conducted from Oc output axons. Together with the presence of temporal jitter at high shock rates, the data suggest the possibility that at least some of the shock-evoked spikes may be generated by excitatory synaptic input to the Oc neurons, most likely from the collaterals of the medial olivocochlear system (MOCS), whose axons pass close to the floor of the IVth ventricle. This excitatory synaptic input may operate to modulate the activity of Oc neurons in addition to MOCS actions in the auditory periphery.







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