Gigantocellular vasodepressor area is tonically active and distinct
from caudal ventrolateral vasodepressor area.
Aicher, Sue A., and Donald J. Reis.
Division of Neurobiology, Cornell University Medical College, 411
E. 69th Street, New York, NY 10021, Phone:(212) 570-2900, FAX:(212)
988-3672
APStracts 3:0346R, 1996.
The Gigantocellular Depressor Area (GiDA) is a functionally-defined
subdivision of the medullary gigantocellular reticular formation
where vasodepressor responses are evoked by glutamate microinjections
(4). The present experiments sought to determine whether the GiDA:
(a) tonically inhibits the sympathetic nervous system; (b) is
necessary for baroreflex function; and (c) 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. Since the effects of GiDA lesions were
identical to those seen following 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, while 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.
Received 10 April 1996; accepted in final form 28 August 1996.
APS Manuscript Number R203-6.
Article publication pending Am. J. Physiol. (Regulatory Integrative
Comp. Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 19 September 1996