Regulation of autonomic nerve activities by central pituitary adenylate cyclase-activating polypeptide

Tanida, Mamoru; Shintani, Norihito; Morita, Yoshiko; Tsukiyama, Naohiro; Hatanaka, Michiyoshi; Hashimoto, Hitoshi; Sawai, Hirozumi; Baba, Akemichi; Nonomura, Katsuya

doi:10.1016/j.regpep.2010.02.002

Cited by 40 publications

(20 citation statements)

References 28 publications

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“…Numerous other studies have linked PACAP with autonomic activation, including those showing PACAP synapsing onto PVN neurons, which are known to control autonomic nervous system activity (14,22,34). Also, intracerebroventricular injection of PACAP in anesthetized rats alters autonomic nerve activity (54), which can be blocked by the melanocortin receptor antagonist SHU9119 (53), further supporting that PACAPmediated effects on energy are at least partially dependent on melanocortin signaling. Interestingly, PACAP knockout mice are highly thermosensitive and require higher ambient temperatures to survive into adulthood, adding to the evidence that PACAP plays a necessary role in thermoregulation (1, 20, 21).…”

Section: Discussionmentioning

confidence: 83%

“…PAC1R is a G protein-coupled receptor that can stimulate adenylate cyclase activity; however, the receptor is heavily alternatively spliced, and several PAC1R splice variants have been shown to activate other secondary messenger pathways (57). Much of the work thus far involving PACAP and feeding behavior has focused on intracerebroventricular injections or global knockouts, neither of which can speak to specific sites of action by which PACAP induces its effects (1,27,38,41,45,53,54,56). PACAP administered intracerebroventricularly produces a robust decrease in food intake with the accompaniment of increased energy expenditure (7,27,38,41,45).…”

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confidence: 99%

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Stimulation of the hypothalamic ventromedial nuclei by pituitary adenylate cyclase-activating polypeptide induces hypophagia and thermogenesis

Resch

Boisvert

Hourigan

et al. 2011

American Journal of Physiology-Regulatory, Integrative and Comp

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Numerous studies have demonstrated that the hypothalamic ventromedial nuclei (VMN) regulate energy homeostasis by integrating and utilizing behavioral and metabolic mechanisms. The VMN heavily express pituitary adenylate cyclase-activating polypeptide (PACAP) type I receptors (PAC1R). Despite the receptor distribution, most PACAP experiments investigating affects on feeding have focused on intracerebroventricular administration or global knockout mice. To identify the specific contribution of PACAP signaling in the VMN, we injected PACAP directly into the VMN and measured feeding behavior and indices of energy expenditure. Following an acute injection of PACAP, nocturnal food intake was significantly reduced for 6 h after injections without evidence of malaise. In addition, PACAP-induced suppression of feeding also occurred following an overnight fast and could be blocked by a specific PAC1R antagonist. Metabolically, VMN-specific injections of PACAP significantly increased both core body temperature and spontaneous locomotor activity with a concurrent increase in brown adipose uncoupling protein 1 mRNA expression. To determine which signaling pathways were responsive to PACAP administration into the VMN, we measured mRNA expression of well-characterized hypothalamic neuropeptide regulators of feeding. One hour after PACAP administration, expression of pro-opiomelanocortin mRNA was significantly increased in the arcuate nuclei (ARC), with no changes in neuropeptide Y and agouti-related polypeptide mRNA levels. This suggests that PAC1R expressing VMN neurons projecting to pro-opiomelanocortin neurons contribute to hypophagia by involving melanocortin signaling. While the VMN also abundantly express PACAP protein, the present study demonstrates that PACAP input to the VMN can influence the control of energy homeostasis.

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Section: Discussionmentioning

confidence: 83%

mentioning

confidence: 99%

Stimulation of the hypothalamic ventromedial nuclei by pituitary adenylate cyclase-activating polypeptide induces hypophagia and thermogenesis

Resch

Boisvert

Hourigan

et al. 2011

American Journal of Physiology-Regulatory, Integrative and Comp

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“…However, PACAP may also have direct actions on anterior pituitary corticotrophs for ACTH release and facilitate posterior pituitary vasopressin secretion (11, 32); interestingly, the adrenal glomerulosa does not express PACAP/VIP receptors suggesting that PACAP-induced glucocorticoid release is driven predominantly by enhanced HPA activity. In addition to enhanced glucocorticoid release (33), central PACAP administration can also lead to sympathetic activation (30, 34) suggesting PACAP can regulate central autonomic pathways. In addition, PACAP is found in preganglionic sympathetic neurons in the intermediolateral cell column of the thoracolumbar spinal cord and accordingly, PACAPergic fibers densely innervate sympathetic ganglia.…”

Section: Pacap and The Stress Responsementioning

confidence: 99%

Pituitary Adenylate Cyclase Activating Polypeptide in Stress-Related Disorders: Data Convergence from Animal and Human Studies

Hammack

May

2015

Biological Psychiatry

106

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The maladaptive expression and function of several stress-associated hormones have been implicated in pathological stress- and anxiety-related disorders. Among these, recent evidence has suggested that pituitary adenylate cyclase activating polypeptide (PACAP) has critical roles in central neurocircuits mediating stress-related emotional behaviors. We describe the PACAPergic systems, the data implicating PACAP in stress biology and how altered PACAP expression and signaling may result in psychopathologies. We include our work implicating PACAP signaling within the bed nucleus of the stria terminalis (BNST) in mediating the consequences of stressor exposure and relatedly, describe more recent studies suggesting that PACAP in the central nucleus of the amygdala (CeA) may impact the emotional aspects of chronic pain states. In aggregate, these results are consistent with data suggesting that PACAP dysregulation is associated with post-traumatic stress disorder (PTSD) in humans.

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“…Central PACAP was found to regulate homeostatic functions such as appetite (Mounien et al, 2009), body temperature (Hawke et al, 2009; Resch et al, 2011), energy metabolism (Inglott et al, 2011), the cardiovascular system (Tanida et al, 2010; Farnham et al, 2012), and the autonomic nervous system (Tanida et al, 2010). In particular, we recently found that intracerebroventricular (ICV) injection of PACAP stimulated SNA to the kidney and adipose tissue, and raised arterial pressure in anesthetized rats (Tanida et al, 2010). Furthermore, sympathetic and hyperglycemic responses to some stressful stimuli including strong light exposure (Hatanaka et al, 2008), immobilization, and/or ether exposure (Tanida et al, 2010) were disrupted in Adcyap1 −/− mice.…”

Section: Introductionmentioning

confidence: 99%

“…In particular, we recently found that intracerebroventricular (ICV) injection of PACAP stimulated SNA to the kidney and adipose tissue, and raised arterial pressure in anesthetized rats (Tanida et al, 2010). Furthermore, sympathetic and hyperglycemic responses to some stressful stimuli including strong light exposure (Hatanaka et al, 2008), immobilization, and/or ether exposure (Tanida et al, 2010) were disrupted in Adcyap1 −/− mice.…”

Section: Introductionmentioning

confidence: 99%

Central PACAP mediates the sympathetic effects of leptin in a tissue-specific manner

et al. 2013

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We previously demonstrated that the peptidergic neurotransmitter pituitary adenylate cyclase-activating polypeptide (PACAP) affects the autonomic system and contributes to the control of metabolic and cardiovascular functions. Previous studies have demonstrated the importance of centrally-mediated sympathetic effects of leptin for obesity-related hypertension. Here we tested whether PACAP signaling in the brain is implicated in leptin-induced sympathetic excitation and appetite suppression. In anesthetized mice, intracerebroventricular (ICV) pre-treatment with PACAP6-38, an antagonist of the PACAP receptors (PAC1-R and VPAC2), inhibited the increase in white adipose tissue sympathetic nerve activity (WAT-SNA) produced by ICV leptin (2 μg). In contrast, leptin-induced stimulation of renal sympathetic nerve activity (RSNA) was not affected by ICV pre-treatment with PACAP6-38. Moreover, in PACAP-deficient (Adcyap1−/−) mice, ICV leptin-induced WAT-SNA increase was impaired, whereas RSNA response was preserved. The reductions in food intake and body weight evoked by ICV leptin were attenuated in Adcyap1−/− mice. Our data suggest that hypothalamic PACAP signaling plays a key role in the control by leptin of feeding behavior and lipocatabolic sympathetic outflow, but spares the renal sympathetic traffic.

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Regulation of autonomic nerve activities by central pituitary adenylate cyclase-activating polypeptide

Cited by 40 publications

References 28 publications

Stimulation of the hypothalamic ventromedial nuclei by pituitary adenylate cyclase-activating polypeptide induces hypophagia and thermogenesis

Stimulation of the hypothalamic ventromedial nuclei by pituitary adenylate cyclase-activating polypeptide induces hypophagia and thermogenesis

Pituitary Adenylate Cyclase Activating Polypeptide in Stress-Related Disorders: Data Convergence from Animal and Human Studies

Central PACAP mediates the sympathetic effects of leptin in a tissue-specific manner

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