Nucleus of the solitary tract catecholaminergic neurons modulate the cardiovascular response to psychological stress in rats

Abstract

Catecholaminergic neurons within the central nervous system are an integral part of stress-related neurocircuitry, and the nucleus of the solitary tract (NTS) plays a critical role in cardiovascular regulation. We tested the hypothesis that NTS catecholaminergic neurons attenuate psychological stress-induced increases in blood pressure and promote neuroendocrine activation in response to psychological stress.Anti-dopamine-β-hydroxylase antibody conjugated to the neurotoxin saporin (DSAP) or saline vehicle was microinjected into the NTS to lesion catecholaminergic neurons in male Sprague-Dawley rats, and 17 days later the rats were subjected to 60 min of restraint stress for five consecutive days. DSAP treatment significantly enhanced the integrated increase in mean arterial pressure during restraint on the first (800 ± 128 and 1115 ± 116 mmHg (min) for saline- and DSAP-treated rats) and fifth days (655 ± 116 and 1035 ± 113 mmHg (min) for saline- and DSAP-treated rats; P<0.01 for overall effect of DSAP treatment) of restraint. In contrast, after 60 min of restraint plasma corticosterone concentration was significantly lower in DSAP-treated compared with saline-treated rats (25.9 ± 7 compared with 46.8 ± 7 μg dl(-1) for DSAP- and saline-treated rats; P <0.05). DSAP treatment also significantly reduced baseline plasma adrenaline concentration (403 ± 69 compared with 73 ± 29 pg ml(-1) for saline- and DSAP-treated rats), but did not alter the magnitude of the adrenaline response to restraint. The data suggest that NTS catecholaminergic neurons normally inhibit the arterial pressure response, but help maintain the corticosterone response to restraint stress.

Role of nucleus of the solitary tract noradrenergic neurons in post-stress cardiovascular and hormonal control in male rats

“…Our results indicate that A2 cells are required for HPA axis responses to psychological stress (i.e., blunted corticosterone response at 30 min after initiation of restraint), probably through (partial) denervation of mpPVN CRH neurons. Our findings are in agreement with previous evidence reporting attenuated restraint-induced Fos immunoreactivity in PVN neurons following total NTS lesion (Dayas et al, 2001) and decreased plasma corticosterone level during restraint following anti-dopamine-b-hydroxylase saporin (DSAP) lesions of the NTS (Daubert et al, 2012). …”

“…These findings are in agreement with reports showing no MAP change after NTS lesions (Itoh et al, 1992; Lin et al, 2013, Snyder et al, 1978, Talman et al, 1980). However, we should note that other studies indicate increased MAP (Daubert et al, 2012; Duale et al, 2007) after NTS cell loss. This apparent contradiction may be due to unequal extent of A2 lesion or to damage to the NTS astrocytes, which play a critical role in mediating cardiovascular reflexes (Lin et al, 2013).…”

“…Stress responses are initiated in part by brainstem noradrenergic (NA) neurons in the nucleus of the solitary tract (A2 region), as depletion of A2 NA neurons reduces pressor responses to psychosocial stressors (Daubert et al, 2012). Cardiovascular stress responses are likely mediated by rich A2 projections to central cardioregulatory circuits, including the ventrolateral medulla (Ross et al, 1985), preautonomic subdivisions of hypothalamic paraventricular nucleus (PVN) and/or the anteroventral subdivisions of the bed nucleus of the stria terminalis (BST) (Ricardo and Koh, 1978; Sawchenko and Swanson, 1982; Riche et al, 1990).…”

Glucocorticoid receptors in the nucleus of the solitary tract (NTS) decrease endocrine and behavioral stress responses

“…Prior studies suggest that NTS projections are not required for regulation of psychogenic stress responses (e.g., footshock, swim); however, more recent studies have cast some doubts on this conclusion, given that 1) DSAP lesion of the NTS reduces the corticosterone response to acute restraint (Daubert et al, 2012) and 2) restraint-induced Fos immunoreactivity in the PVN neurons is decreased after ibotenate lesion of NTS (Dayas et al, 2001). Our data further suggest that ascending activation of the HPA axis by the NTS is subject to regulation by glucocorticoids, presumably as a feedback mechanism to decrease excitatory drive to the PVN.…”

Protein expression levels in the medullary visceral zone of rats with subarachnoid hemorrhage

“…Its expression was more intensive in the NTS and ventrolateral medulla, in which 50% of neurons were MVZ/tyrosine hydroxylase double-positive, indicating that the catecholaminergic neurons in MVZ are involved in the stress response to cardiovascular noxious stimuli (Rotoli et al, 2011;Daubert et al, 2012). In view of the limited experimental conditions, this study did not investigate the changes of blood pressure and electrocardiogram measurements in the rats after SAH, but the changes in heart rate and myocardial enzymes did reflect myocardial ischemia.…”