Modulation of sympathetic discharge by a hypothalamic GABAergic mechanism.
Recent studies have shown that a GABAergic mechanism in the posterior hypothalamus modulates tonic levels of arterial pressure and heart rate and the bradycardiac response to baroreceptor stimulation. It has not been determined if this modulation involves an alteration of sympathetic discharge by an effect upon hypothalamic neurons. Therefore, the purpose of the present study was to determine if manipulation of GABAergic activity in the posterior hypothalamus altered sympathetic nerve discharge. Cervical nerve activity was recorded and processed as an indication of sympathetic activity in anesthetized, ventilated cats. Unilateral injections of a GABA antagonist (picrotoxin) into the posterior hypothalamus produced increases in both rhythmic and tonic sympathetic discharge, with concomitant increases in arterial pressure and heart rate. These responses were reversed by injections of a GABA agonist (muscimol) into the same site. Injections of the vehicle solution (Ringers) or muscimol without a prior injection of picrotoxin had no effect upon the sympathetic discharge. These results suggest that a GABAergic mechanism exerts a tonic inhibitory effect upon sympathetic discharge by an action in the posterior hypothalamus.[1]References
- Modulation of sympathetic discharge by a hypothalamic GABAergic mechanism. Waldrop, T.G., Bauer, R.M. Neuropharmacology (1989) [Pubmed]
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