Circadian rhythms in physiology and behavior are temporally synchronized to the day/night cycle through the action of light on the circadian clock. In mammals, transduction of the photic signal reaching the circadian oscillator in the suprachiasmatic nucleus (SCN) occurs through the release of glutamate and pituitary adenylate cyclase-activating peptide (PACAP). The authors' study aimed at clarifying the role played by PACAP in photic resetting and entrainment. They investigated the circadian response to light of PACAPnullmice lacking the 5th exon of the PACAP coding sequence. Specifically, they examined free-running rhythms, entrainment to 12-h light:12-h dark (LD)cycles, the phase-response curve (PRC) to single light pulses, entrainment to a23-h T-cycle, re-entrainment to 6-h phase shifts in LD cycles, and light-induced c-Fos expression. PACAP-null and wild-type mice show similar free-running periods and similar entrainment to 12:12 LD cycles. However, the PRC of PACAP-null mice lacks a phase-advance portion. Surprisingly, despite the absence of phase advance to single light pulses, PACAP-null mice are able to entrain to a 23-h T-cycle, but with a significantly longer phase angle of entrainment than wild types. In addition, PACAP-null mice re-entrain more slowly to a 6-h phase advance of the LD cycle. Nevertheless, induction of c-Fos by light in late night is normal. In all experiments, PACAP-null mice show specific behavioral impairments in response to phase-advancing photic stimuli. These results suggest that PACAP is required for the normal integration of the phase advancing light signal by the SCN.
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http://dx.doi.org/10.1177/0748730409332037 | DOI Listing |
J Neuroendocrinol
November 2023
Section on Molecular Neuroscience, National Institute of Mental Heath - Intramural Research Program, Bethesda, Maryland, USA.
Neuropeptides may exert trophic effects during development, and then neurotransmitter roles in the developed nervous system. One way to associate peptide-deficiency phenotypes with either role is first to assess potential phenotypes in so-called constitutive knockout mice, and then proceed to specify, regionally and temporally, where and when neuropeptide expression is required to prevent these phenotypes. We have previously demonstrated that the well-known constellation of behavioral and metabolic phenotypes associated with constitutive pituitary adenylate cyclase-activating peptide (PACAP) knockout mice are accompanied by transcriptomic alterations of two types: those that distinguish the PACAP-null phenotype from wild-type (WT) in otherwise quiescent mice (cPRGs), and gene induction that occurs in response to acute environmental perturbation in WT mice that do not occur in knockout mice (aPRGs).
View Article and Find Full Text PDFAm J Physiol Endocrinol Metab
March 2021
Northern Medical Program, University of Northern British Columbia, Prince George, British Columbia, Canada.
Pituitary adenylate cyclase-activating polypeptide (PACAP) is a neuropeptide critical to the regulation of the stress response, including having a role in energy homeostasis. Mice lacking PACAP are cold-sensitive and have impaired adrenergic-induced thermogenesis. Interestingly, null mice can survive cold housing if acclimated slowly, similar to observations in uncoupling protein 1 (UCP1)-deficient mice.
View Article and Find Full Text PDFExp Physiol
February 2021
Northern Medical Program, University of Northern British Columbia, Prince George, British Columbia, Canada.
New Findings: What is the central question of this study? Can chronic treatment of pituitary adenylate cyclase-activating polypeptide (PACAP) deficient mice with the melanocortin agonist melanotan II during cold acclimation rescue the impaired thermogenic capacity previously observed in PACAP deficient mice? What is the main finding and its importance? Using a genetic model of PACAP deficiency, this study provides evidence that PACAP acts upstream of the melanocortin system in regulating sympathetic nerve activity to brown adipose tissue in mice.
Abstract: Impaired adipose tissue function in obesity, including reduced thermogenic potential, has detrimental consequences for metabolic health. Hormonal regulation of adaptive thermogenesis is being explored as a potential therapeutic target for human obesity.
Front Neurosci
December 2019
Neuroscience Program, University of Illinois at Urbana-Champaign, Urbana, IL, United States.
Results from a variety of sources indicate a role for pituitary adenylate cyclase-activating polypeptide (PACAP) in light/glutamate-induced phase resetting of the circadian clock mediated by the retinohypothalamic tract (RHT). Attempts to block or remove PACAP's contribution to clock-resetting have generated phenotypes that differ in their responses to light or glutamate. For example, previous studies of circadian behaviors found that period-maintenance and early-night phase delays are intact in PACAP-null mice, yet there is a consistent deficit in behavioral phase-resetting to light stimulation in the late night.
View Article and Find Full Text PDFNihon Yakurigaku Zasshi
May 2019
Faculty of Science, Graduate School of Science and Engineering, University of Toyama.
Dry eye syndrome is defined as a disorder of the tear film caused by either a decreased production in tears or a disruption to the stability of the complex tear film, which causes damage to the ocular surface. It has been developed the medicine for dry eye syndrome focusing anti-inflammation or mucin secretion, however, no treatment has been developed focusing on the effect of elevation of the lacrimal secretion. We recently identified that pituitary adenylate cyclase-activating polypeptide (PACAP)-null mice develop dry eye-like symptoms such as corneal keratinization and tear reduction.
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