Limits...
Hydration and beyond: neuropeptides as mediators of hydromineral balance, anxiety and stress-responsiveness.

Smith JA, Pati D, Wang L, de Kloet AD, Frazier CJ, Krause EG - Front Syst Neurosci (2015)

Bottom Line: Challenges to body fluid homeostasis can have a profound impact on hypothalamic regulation of stress responsiveness.Interestingly, following exposure to perceived threats to homeostasis, select limbic brain regions mediate behavioral and physiological responses to psychogenic stressors, in part, by influencing activation of the same PVH neurons that are known to maintain body fluid homeostasis.Here, we review past and present research examining interactions between hypothalamic circuits regulating body fluid homeostasis and those mediating behavioral and physiological responses to psychogenic stress.

View Article: PubMed Central - PubMed

Affiliation: Laboratory of Dr. Eric Krause, Department of Pharmacodynamics, College of Pharmacy, University of Florida Gainesville, FL, USA.

ABSTRACT
Challenges to body fluid homeostasis can have a profound impact on hypothalamic regulation of stress responsiveness. Deficiencies in blood volume or sodium concentration leads to the generation of neural and humoral signals relayed through the hindbrain and circumventricular organs that apprise the paraventricular nucleus of the hypothalamus (PVH) of hydromineral imbalance. Collectively, these neural and humoral signals converge onto PVH neurons, including those that express corticotrophin-releasing factor (CRF), oxytocin (OT), and vasopressin, to influence their activity and initiate compensatory responses that alleviate hydromineral imbalance. Interestingly, following exposure to perceived threats to homeostasis, select limbic brain regions mediate behavioral and physiological responses to psychogenic stressors, in part, by influencing activation of the same PVH neurons that are known to maintain body fluid homeostasis. Here, we review past and present research examining interactions between hypothalamic circuits regulating body fluid homeostasis and those mediating behavioral and physiological responses to psychogenic stress.

No MeSH data available.


Related in: MedlinePlus

2.0 M NaCl administration and restraint increases activation of OT-producing cells in the paraventricular nucleus of the hypothalamus (PVH). (A) Representative photomicrograph of a unilateral coronal section depicting Fos induction (red nuclei) in OT (green cell bodies) containing neurons following 0.15 M NaCl and restraint. (B) Representative photomicrograph of a unilateral coronal section depicting Fos induction in OT neurons following 2.0 M NaCl and restraint. (C) The group mean for Fos induction in OT-producing cells was significantly more for mice subjected to 2.0 M NaCl injection and restraint relative to control. *p < 0.05 Scale bars = 50 μm. Reprinted with permission from Smith et al. (2014).
© Copyright Policy - open-access
Related In: Results  -  Collection

License
getmorefigures.php?uid=PMC4379895&req=5

Figure 5: 2.0 M NaCl administration and restraint increases activation of OT-producing cells in the paraventricular nucleus of the hypothalamus (PVH). (A) Representative photomicrograph of a unilateral coronal section depicting Fos induction (red nuclei) in OT (green cell bodies) containing neurons following 0.15 M NaCl and restraint. (B) Representative photomicrograph of a unilateral coronal section depicting Fos induction in OT neurons following 2.0 M NaCl and restraint. (C) The group mean for Fos induction in OT-producing cells was significantly more for mice subjected to 2.0 M NaCl injection and restraint relative to control. *p < 0.05 Scale bars = 50 μm. Reprinted with permission from Smith et al. (2014).

Mentions: Recent investigation into the effects of hypertonic saline injection on humoral, behavioral, and central measures of stress responsiveness in male rats and mice revealed a prominent role for activation of oxytocinergic pathways. Hypertonic (2.0 M) saline injected s.c. followed by 60 min water deprivation resulted in decreased ACTH, glucocorticoid, and PRA during a 60 min restraint period, but significantly increased plasma OT levels (Krause et al., 2011a; See Figure 3). Cardiovascular recordings determined that rats rendered mildly hypernatremic and subsequently exposed to restraint stress had mean arterial pressure and heart-rate variability return to pre-restraint levels faster than normonatremic controls (Krause et al., 2011a). Consistent with previous reports (Pirnik et al., 2004) acute hypernatremia increased Fos induction in AVP and OT expressing neurons in the PVH and SON, an effect that was predictive of increased social interactions but decreased anxiety-like behavior in the elevated plus maze (Krause et al., 2011a). Acute hypernatremia and restraint stress interacted to increase Fos expression in the OVLT, oval capsule of the BNST, ventral lateral septum, and central nucleus of the amygdala (Frazier et al., 2013). However, the increased neuronal activation that occurred subsequent to acute hypernatremia and restraint was specific to these brain regions as the medial pre-frontal cortex, lateral ventral BNST, and dorsomedial hypothalamus showed no significant change in Fos expression (Frazier et al., 2013). Whole cell patch clamp recordings revealed that acute hypernatremia caused inhibition of CRF neurons in the PVH that was dependent on activation of OT receptors (Frazier et al., 2013; Figure 4). Follow-up studies utilized the Cre-lox system to generate a line of CRF reporter mice to investigate the mechanisms underlying the anxiolysis and HPA dampening that accompanies acute hypernatremia (Smith et al., 2014). Acute hypernatremia elicited robust activation of OT neurons in the PVH but attenuated the Fos induction that occurs in CRF neurons subsequent to restraint stress (Smith et al., 2014; See Figures 5, 6), suggesting that the oxytocinergic tone that inhibited CRF neurons in electrophysiological experiments suppresses stress-induced activation of CRF neurons in vivo.


Hydration and beyond: neuropeptides as mediators of hydromineral balance, anxiety and stress-responsiveness.

Smith JA, Pati D, Wang L, de Kloet AD, Frazier CJ, Krause EG - Front Syst Neurosci (2015)

2.0 M NaCl administration and restraint increases activation of OT-producing cells in the paraventricular nucleus of the hypothalamus (PVH). (A) Representative photomicrograph of a unilateral coronal section depicting Fos induction (red nuclei) in OT (green cell bodies) containing neurons following 0.15 M NaCl and restraint. (B) Representative photomicrograph of a unilateral coronal section depicting Fos induction in OT neurons following 2.0 M NaCl and restraint. (C) The group mean for Fos induction in OT-producing cells was significantly more for mice subjected to 2.0 M NaCl injection and restraint relative to control. *p < 0.05 Scale bars = 50 μm. Reprinted with permission from Smith et al. (2014).
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4379895&req=5

Figure 5: 2.0 M NaCl administration and restraint increases activation of OT-producing cells in the paraventricular nucleus of the hypothalamus (PVH). (A) Representative photomicrograph of a unilateral coronal section depicting Fos induction (red nuclei) in OT (green cell bodies) containing neurons following 0.15 M NaCl and restraint. (B) Representative photomicrograph of a unilateral coronal section depicting Fos induction in OT neurons following 2.0 M NaCl and restraint. (C) The group mean for Fos induction in OT-producing cells was significantly more for mice subjected to 2.0 M NaCl injection and restraint relative to control. *p < 0.05 Scale bars = 50 μm. Reprinted with permission from Smith et al. (2014).
Mentions: Recent investigation into the effects of hypertonic saline injection on humoral, behavioral, and central measures of stress responsiveness in male rats and mice revealed a prominent role for activation of oxytocinergic pathways. Hypertonic (2.0 M) saline injected s.c. followed by 60 min water deprivation resulted in decreased ACTH, glucocorticoid, and PRA during a 60 min restraint period, but significantly increased plasma OT levels (Krause et al., 2011a; See Figure 3). Cardiovascular recordings determined that rats rendered mildly hypernatremic and subsequently exposed to restraint stress had mean arterial pressure and heart-rate variability return to pre-restraint levels faster than normonatremic controls (Krause et al., 2011a). Consistent with previous reports (Pirnik et al., 2004) acute hypernatremia increased Fos induction in AVP and OT expressing neurons in the PVH and SON, an effect that was predictive of increased social interactions but decreased anxiety-like behavior in the elevated plus maze (Krause et al., 2011a). Acute hypernatremia and restraint stress interacted to increase Fos expression in the OVLT, oval capsule of the BNST, ventral lateral septum, and central nucleus of the amygdala (Frazier et al., 2013). However, the increased neuronal activation that occurred subsequent to acute hypernatremia and restraint was specific to these brain regions as the medial pre-frontal cortex, lateral ventral BNST, and dorsomedial hypothalamus showed no significant change in Fos expression (Frazier et al., 2013). Whole cell patch clamp recordings revealed that acute hypernatremia caused inhibition of CRF neurons in the PVH that was dependent on activation of OT receptors (Frazier et al., 2013; Figure 4). Follow-up studies utilized the Cre-lox system to generate a line of CRF reporter mice to investigate the mechanisms underlying the anxiolysis and HPA dampening that accompanies acute hypernatremia (Smith et al., 2014). Acute hypernatremia elicited robust activation of OT neurons in the PVH but attenuated the Fos induction that occurs in CRF neurons subsequent to restraint stress (Smith et al., 2014; See Figures 5, 6), suggesting that the oxytocinergic tone that inhibited CRF neurons in electrophysiological experiments suppresses stress-induced activation of CRF neurons in vivo.

Bottom Line: Challenges to body fluid homeostasis can have a profound impact on hypothalamic regulation of stress responsiveness.Interestingly, following exposure to perceived threats to homeostasis, select limbic brain regions mediate behavioral and physiological responses to psychogenic stressors, in part, by influencing activation of the same PVH neurons that are known to maintain body fluid homeostasis.Here, we review past and present research examining interactions between hypothalamic circuits regulating body fluid homeostasis and those mediating behavioral and physiological responses to psychogenic stress.

View Article: PubMed Central - PubMed

Affiliation: Laboratory of Dr. Eric Krause, Department of Pharmacodynamics, College of Pharmacy, University of Florida Gainesville, FL, USA.

ABSTRACT
Challenges to body fluid homeostasis can have a profound impact on hypothalamic regulation of stress responsiveness. Deficiencies in blood volume or sodium concentration leads to the generation of neural and humoral signals relayed through the hindbrain and circumventricular organs that apprise the paraventricular nucleus of the hypothalamus (PVH) of hydromineral imbalance. Collectively, these neural and humoral signals converge onto PVH neurons, including those that express corticotrophin-releasing factor (CRF), oxytocin (OT), and vasopressin, to influence their activity and initiate compensatory responses that alleviate hydromineral imbalance. Interestingly, following exposure to perceived threats to homeostasis, select limbic brain regions mediate behavioral and physiological responses to psychogenic stressors, in part, by influencing activation of the same PVH neurons that are known to maintain body fluid homeostasis. Here, we review past and present research examining interactions between hypothalamic circuits regulating body fluid homeostasis and those mediating behavioral and physiological responses to psychogenic stress.

No MeSH data available.


Related in: MedlinePlus