Nodulus-uvula depressor response: central GABA-mediated inhibition of alpha-adrenergic outflow.
Electrical stimulation of a lateral region of the cerebellar nodulus-uvula transition zone in anesthetized albino rabbits decreases mean arterial blood pressure in direct proportion to stimulus intensity. The hypotension has an abrupt onset and is phasic; heart rate is unaffected. Neural pathways that might mediate the depressor response were studied using autonomic-blocking agents. Pretreatment with 2 mg/kg iv of either propranolol HCl or atropine methyl nitrate did not alter the onset or duration of the hypotensive response. However, pretreatment with 2 mg/kg iv phentolamine HCl abolished the depressor response, and 7 mg.kg-1.min-1 iv tetraethylammonium infusion decreased the response by more than 50%. Ipsilateral injections of 200 ng bicuculline methiodide into an area immediately dorsal to the superior cerebellar peduncle or the dorsal aspect of the superior vestibular nucleus reversibly attenuated the nodulus-uvula evoked depression. Anterograde horseradish peroxidase-wheat germ agglutinin (HRP-WGA) transport experiments revealed that both these regions receive direct inputs from the nodulus-uvula. These data suggest that hypotensive events elicited by lateral nodulus-uvula stimuli represent a central, alpha-aminobutyric acid-mediated, phasic inhibition of vasomotor drive mediated through autonomic ganglia to alpha-adrenoreceptors in the vasculature.[1]References
- Nodulus-uvula depressor response: central GABA-mediated inhibition of alpha-adrenergic outflow. Henry, R.T., Connor, J.D., Balaban, C.D. Am. J. Physiol. (1989) [Pubmed]
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