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AJP - Regulatory, Integrative and Comparative Physiology, Vol 254, Issue 2 257-R267, Copyright © 1988 by American Physiological Society
ARTICLES |
K. J. Varner, S. M. Barman and G. L. Gebber
Department of Pharmacology and Toxicology, Michigan State University, East Lansing 48824.
In a companion paper, we demonstrated that hypothalamic or medial thalamic lesions attenuate the reduction in inferior cardiac postganglionic sympathetic nerve discharge (SND) produced by decerebration in the anesthetized cat [Huang et al., Am. J. Physiol. 254 (Regulatory Integrative Comp. Physiol. 23): R249-R256, 1988]. This raised the possibility that these diencephalic regions contain the cell bodies of neurons that contribute to SND. The current study tested this possibility in cats anesthetized with alpha-chloralose. Spike-triggered averaging of inferior cardiac SND revealed the existence of two types of hypothalamic and medial thalamic neurons with sympathetic nerve-related activity. Recordings were made from the soma-dendritic region of these neurons, since an inflection often appeared on the rising phase of the unit action potential. The activity of type 1 neurons was synchronized to an aperiodic spikelike event in SND, whereas that of type 2 neurons was synchronized to a 2- to 6-Hz rhythmic component. Some of the type 2 neurons but none of the type 1 neurons had cardiac-related activity. Microstimulation at type 1 and type 2 unit recording sites increased SND. Our results are consistent with the possibility that hypothalamic and medial thalamic neurons contribute to the rhythmic and aperiodic components of SND in the anesthetized cat.
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