Gigantocellular vasodepressor area is tonically active and distinct from caudal ventrolateral vasodepressor area.
The gigantocellular depressor area (GiDA) is a functionally defined subdivision of the medullary gigantocellular reticular formation where vasodepressor responses are evoked by glutamate microinjections (Aicher, S. A., D. J. Reis, D. A. Ruggiero, and T. A. Milner. Neuroscience 60: 761-779, 1994). The present experiments sought to determine whether the GiDA 1) tonically inhibits the sympathetic nervous system; 2) is necessary for baroreflex function; and 3) is functionally distinct from adjacent vasodepressor regions in the medullary reticular formation, including the midline raphe nuclei and the caudal ventrolateral medulla (CVL). Excitotoxic lesions of the GiDA abolished the baroreflex and significantly increased sympathetic nerve activity in anesthetized rats. Equivalent injections into the midline raphe nuclei elevated sympathetic activity but did not alter baroreflex responses. Therefore, the GiDA is functionally distinct from the raphe nuclei, although both contain tonically active sympathoinhibitory neurons. Because the effects of GiDA lesions were identical to those seen after lesions of the CVL, further studies were required to demonstrate that the GiDA and CVL are functionally and anatomically distinct. First, intramedullary injections of kynurenic acid produced hypertension and blocked the baroreflex when placed in the CVL, but not when placed in the GiDA. Second, muscimol inactivation of the RVL blocked the hypertension produced by excitotoxic lesions of the CVL, but failed to block the hypertension produced by similar lesions of the GiDA. Third, CVL neurons project to the RVL but not the spinal cord, whereas GiDA neurons project to the spinal cord but not the RVL. These studies show that the CVL and GiDA are both tonically sympathoinhibitory regions, but they are distinct with regard to their functional connectivity with other autonomic regions.
Aicher
S A
SA
Division of Neurobiology, Cornell University Medical College, New York, New York 10021, USA.
Reis
D J
DJ
D000344:Afferent Pathways / Q000187:drug effects / Q000502:physiology; D000818:Animals; D001011:Aorta / Q000294:innervation; D017704:Baroreflex / Q000187:drug effects; D001794:Blood Pressure / Q000187:drug effects; D001931:Brain Mapping; D004525:Efferent Pathways / Q000187:drug effects / Q000502:physiology; D004558:Electric Stimulation; D018698:Glutamic Acid / Q000008:administration & dosage / Q000494:pharmacology*; D007608:Kainic Acid / Q000008:administration & dosage / Q000494:pharmacology; D007736:Kynurenic Acid / Q000008:administration & dosage / Q000494:pharmacology; D008297:Male; D008526:Medulla Oblongata / Q000187:drug effects / Q000502:physiology*; D008845:Microinjections; D009118:Muscimol / Q000008:administration & dosage / Q000494:pharmacology; D010656:Phenylephrine / Q000008:administration & dosage / Q000494:pharmacology; D011903:Raphe Nuclei / Q000187:drug effects / Q000502:physiology; D051381:Rats; D017207:Rats, Sprague-Dawley; D012154:Reticular Formation / Q000502:physiology*; D013564:Sympathetic Nervous System / Q000502:physiology; D014666:Vasomotor System / Q000502:physiology*
D010656:Phenylephrine; D009118:Muscimol; D018698:Glutamic Acid; D007736:Kynurenic Acid; D007608:Kainic Acid