Journal article
Central PACAP mediates the sympathetic effects of leptin in a tissue-specific manner
Neuroscience, Vol.238, pp.297-304
05/15/2013
DOI: 10.1016/j.neuroscience.2013.02.016
PMCID: PMC5684871
PMID: 23454538
Abstract
► Possible role of central PACAP signaling in sympathetic regulation by leptin. ► Sympathetic and feeding regulation by leptin and PACAP signaling. ► Central PACAP contributes to sympathetic and feeding actions of leptin.
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 (2μg). 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.
Details
- Title: Subtitle
- Central PACAP mediates the sympathetic effects of leptin in a tissue-specific manner
- Creators
- M Tanida - Department of Biomedical Sciences, College of Life Sciences, Ritsumeikan University, Kusatsu, Shiga 525-8577, JapanA Hayata - Laboratory of Molecular Neuropharmacology, Graduate School of Pharmaceutical Sciences, Osaka University, 1-6 Yamadaoka, Suita, Osaka 565-0871, JapanN Shintani - Laboratory of Molecular Neuropharmacology, Graduate School of Pharmaceutical Sciences, Osaka University, 1-6 Yamadaoka, Suita, Osaka 565-0871, JapanN Yamamoto - College of Pharmacology, Ritsumeikan University, Kusatsu, Shiga 525-8577, JapanY Kurata - Department of Physiology II, Kanazawa Medical University, Uchinada, Ishikawa 920-0293, JapanT Shibamoto - Department of Physiology II, Kanazawa Medical University, Uchinada, Ishikawa 920-0293, JapanD.A Morgan - Departments of Pharmacology, University of Iowa Carver, College of Medicine, Iowa City, IA 52242, USAK Rahmouni - Departments of Pharmacology, University of Iowa Carver, College of Medicine, Iowa City, IA 52242, USAH Hashimoto - Laboratory of Molecular Neuropharmacology, Graduate School of Pharmaceutical Sciences, Osaka University, 1-6 Yamadaoka, Suita, Osaka 565-0871, Japan
- Resource Type
- Journal article
- Publication Details
- Neuroscience, Vol.238, pp.297-304
- DOI
- 10.1016/j.neuroscience.2013.02.016
- PMID
- 23454538
- PMCID
- PMC5684871
- NLM abbreviation
- Neuroscience
- ISSN
- 0306-4522
- eISSN
- 1873-7544
- Publisher
- Elsevier Ltd
- Grant note
- DOI: 10.13039/501100001700, name: Ministry of Education, Culture, Sports, Science and Technology, award: 23689008
- Language
- English
- Date published
- 05/15/2013
- Academic Unit
- Iowa Neuroscience Institute; Fraternal Order of Eagles Diabetes Research Center; Neuroscience and Pharmacology; Internal Medicine
- Record Identifier
- 9984040354602771
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