Osmotic regulation of neuronal nitric oxide synthase expression in the rat amygdala: Functional role for nitric oxide in adaptive responses?

✍ Scribed by Song T. Yao; Vagner R. Antunes; Julian F.R. Paton; David Murphy

• Publisher: John Wiley and Sons
• Year: 2007
• Tongue: English
• Weight: 754 KB
• Volume: 85
• Category: Article
• ISSN: 0360-4012
• DOI: 10.1002/jnr.21114

✦ Synopsis

Abstract

Water‐deprivation‐induced osmotic stress leads to activation of a number of adaptive responses. Nitric oxide (NO) has been implicated in the modulation of these responses, as the amygdala has been implicated in ingestive behavior and modulation of autonomic homeostatic functions. Here we investigated the effects of water deprivation on neuronal nitric oxide synthase (nNOS) expression within the rat amygdala; a brain area involved in modulating ingestive behavior and autonomic function. Water deprivation resulted in significant increases in nNOS immunoreactivity (‐ir) within different regions of the amygdala compared with euhydrated rats. Maximal increases were observed in the anteroventral (118 ± 9 vs. 47 ± 3 neurons), anteriodorsal (133 ± 9 vs. 77 ± 3), and posterioventral (175 ± 5 vs. 71 ± 5) parts of the medial amygdala. The basomedial nucleus (65 ± 4 vs. 39 ± 3) and posterior basolateral nucleus (19 ± 2 vs. 5 ± 1) of the amygdala and the capsular (21 ± 2 vs. 6 ± 1) and medial (44 ± 6 vs. 22 ± 3) parts of the central nucleus of the amygdala also showed increased nNOS‐ir in dehydrated rats. Water deprivation had no effect on nNOS‐ir in areas such as the cortical, anterior basolateral, and intercalated nuclei of the amygdala. Microinjection of an NO donor, DEA‐NONOate, into the central amygdala resulted in a pressor and tachycardic response that was attenuated by a soluble guanylate cyclase inhibitor. These observations suggest that activation of the nitrergic system is prevalent throughout the amygdala following water deprivation and suggest that the up‐reguation of nNOS could play a significant role in the integrative response to osmotic stress. © 2006 Wiley‐Liss, Inc.