Specific neuronal phenotypes within the rostral ventrolateral medulla following cardiovascular deconditioning in rats
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[ACCESS RESTRICTED TO THE UNIVERSITY OF MISSOURI AT REQUEST OF AUTHOR.] Humans exposed to prolonged periods of bed rest or spaceflight undergo multiple cardiovascular adaptations including a predisposition for orthostatic intolerance. Studies in both humans and rats suggest there may be alterations within the brain following periods of spaceflight or bed rest. The hindlimb unloaded (HU) rat model shows similar cardiovascular consequences to that of humans and exhibits an attenuated sympathoexcitatory response during a hypotensive stimulus in addition to an enhanced GABAergic ([gamma]-amino butyric-acid) inhibition at the level of the rostral ventrolateral medulla (RVLM). Nitric oxide (NO), a central neuromodulator, has been shown to increase GABA release in the central nervous system. Thus, NO may contribute to the enhanced GABAergic inhibition in the RVLM after HU. The RVLM also contains a population of catecholaminergic cells important for sympathetic nervous system regulation. We hypothesized that 14 days of HU increases the number of neuronal nitric oxide synthase and glutamic acid decarboxylase, 67 kDa isoform, (GAD67) immunoreactive cells and decreases the number of phenylethanolamine N-methyl transferase (PNMT; marker for catecholaminergic cells) cells within the RVLM. The number and distribution of nNOS, GAD67, and PNMT cells were examined using immunohistochemistry in brainstem sections (30 [micrometers]) from control and HU male rats. Contrary to our hypothesis, our results suggest that changes in the number of nNOS or PNMT or GABAergic neurons within the RVLM may not contribute to the increased GABAergic inhibition in the RVLM or the attenuation of reflex activation of sympathetic nervous system activity following 14 days of HU.
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