Role of superior laryngeal nerve and Fos staining following dehydration and rehydration in the rat

Abstract

Immunohistochemistry for Fos was used to determine the role of the superior laryngeal nerve in conscious rats following water deprivation and rehydration. Adult male rats were subjected to either unilateral superior laryngeal nerve section (SLNX) or sham surgery. Two weeks later rats from each surgical group were water deprived for 48 h or water deprived for 46 h hours and given access to water for 2 h prior to perfusion. Controls were allowed ad libitum access to water. Brains were processed for Fos using a commercially available antibody. Changes in plasma osmolality and hematocrit were not significantly different between SLNX and sham following any of the treatments. Water intake in rats was not significantly affected by SLNX. In the supraoptic nucleus (SON) of sham rats, water deprivation significantly increased Fos staining while water intake following dehydration prevented this increase. Water deprivation significantly increased Fos staining in the SON of SLNX rats. Following water intake after 46 h water deprivation in SLNX rats, Fos staining in the ipsilateral SON was significantly greater than the contralateral SON and significantly lower than 48 h water deprivation. In the nucleus of the solitary tract (NTS) of sham rats, both water deprivation and water intake produced significant increases in Fos staining bilaterally compared to euhydrated controls. In SLNX rats, water deprivation significantly increased Fos in both ipsilateral and contralateral NTS that was not different from sham rats. SLNX significantly decreased Fos staining in the ipsilateral NTS of rats given access to water after dehydration compared to the corresponding sham treated rats. Fos staining was not affected in the contralateral NTS of SLNX rats given access to water after dehydration. This suggests that the superior laryngeal nerve contributes to changes in Fos staining in the NTS and SON following water intake in dehydrated rats.

MSG-Evoked c-Fos Activity in the Nucleus of the Solitary Tract Is Dependent upon Fluid Delivery and Stimulation Parameters

“…Although our results are in line with previous research that report increased Fos-LI in the nTS following prolonged water restriction alone (Ji et al 2007;Gottlieb et al 2011), our study has 3 primary advantages over these other studies. First, our study is the first to compare brain activation in response to taste stimulation, as measured by Fos-LI, between water-restricted and water-replete animals.…”

“…In this regard, auditory stimulation patterns are known to influence c-Fos activity in the cerebellum, with faster stimulation patterns (i.e., 40 Hz) producing more c-Fos positive cells than slower stimulation patterns (i.e., 10 Hz; Tian and Bishop 2002). Moreover, dehydration and rehydration are also known to influence c-Fos activity specifically within in the nucleus of the solitary tract (nTS), the primary taste/viscerosensory nucleus (Ji et al 2007;Gottlieb et al 2011). In particular, both prolonged (e.g., >45 h) water deprivation as well as brief rehydration (e.g., <2 h) significantly increase the number of c-Fos as compared with control animals.…”

Mapping brain Fos immunoreactivity in response to water deprivation and partial rehydration: Influence of sodium intake

“…However, ECF repletion was likely not a predominant effect on Fos-ir because of the opposite patterns of Fos-ir produced by water and sodium intake in some areas. Satiety of thirst, or oral and gastrointestinal stimulation produced by water intake may have also induced Fos-ir at the end of WD-PR [25][26][27], but again the effect on brain Fos-ir was different from that produced by sodium intake, suggesting that gastrointestinal fill was not the source of the alteration in Fosir in all areas.…”

Neural Substrate Essential for Suppression of Vasopressin Secretion and Excretion of a Water Load

“…These data also suggest that the suppression of AVP release following rehydration may be caused in part by inhibitory neural influences on the magnocellular vasopressin‐containing neurones of the SON and PVN. The neural pathways that mediate this rapid inhibition of vasopressin release associated with drinking have yet to be defined, although, at the outset, part of the neural signal appears to involve the superior laryngeal nerve in rats . Whether the inhibitory pathway from the MnPO to the SON has a role in drinking‐induced suppression of vasopressin secretion remains to be investigated.…”