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J Neurophysiol 85: 2639-2642, 2001;
0022-3077/01 $5.00
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The Journal of Neurophysiology Vol. 85 No. 6 June 2001, pp. 2639-2642
Copyright ©2001 by the American Physiological Society

RAPID COMMUNICATION

Disynaptic Inhibition of Omnipause Neurons Following Electrical Stimulation of the Superior Colliculus in Alert Cats

Kaoru Yoshida,1 Yoshiki Iwamoto,1 Sohei Chimoto,1 and Hiroshi Shimazu2

 1Department of Physiology, Institute of Basic Medical Sciences, University of Tsukuba, Ibaraki 305-8575; and  2Department of Neurophysiology, Tokyo Metropolitan Institute for Neuroscience, Tokyo 183-8526, Japan

Yoshida, Kaoru, Yoshiki Iwamoto, Sohei Chimoto, and Hiroshi Shimazu. Disynaptic Inhibition of Omnipause Neurons Following Electrical Stimulation of the Superior Colliculus in Alert Cats. J. Neurophysiol. 85: 2639-2642, 2001. We investigated the synaptic organization responsible for the inhibition of omnipause neurons (OPNs) following stimulation of the superior colliculus (SC) in alert cats. Stimulation electrodes were implanted bilaterally in the rostral and caudal SC where a short-pulse train induced small and large saccades, respectively. Effects of single-pulse stimulation on OPNs were examined with intracellular and extracellular recordings. In contrast to monosynaptic excitatory postsynaptic potentials, which were induced by rostral SC stimulation, inhibitory postsynaptic potentials were induced with disynaptic latencies (1.3-1.9 ms) from both the rostral and caudal SC in most OPNs. Analysis of a larger extracellular sample complemented intracellular observations. Monosynaptic activation of OPNs was elicited more frequently from rostral sites than from caudal sites, whereas spike suppression with disynaptic latencies was induced by caudal as well as rostral stimulation with similar frequencies. The results imply that disynaptic inhibition is produced by activation of SC cells that are distributed over wide regions related to saccades of different sizes. We suggest that signals from these neurons initiate a saccadic pause of OPNs through single inhibitory interneurons.




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