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Substance P is associated with hypothalamic paraventricular nucleus activation that coincides with increased
Jacob D Mace1, Tetsuya Tachibana2, Guoqing Wang3
1The Edward Via College of Osteopathic Medicine, Blacksburg, VA, USA.
Insights
Substance P (SP) reduces food intake in chicks by activating the paraventricular nucleus (PVN) in the brain. This mechanism may involve increased expression of urotensin 2 (UTS2) mRNA.
Area of Science:
- Neuroscience
- Endocrinology
- Animal Science
Background:
- Exogenous substance P (SP) administration causes anorexia in chicks and rats.
- The central neural pathways mediating SP-induced anorexia are not well understood.
Purpose of the Study:
- To investigate the central mechanisms underlying substance P (SP)-induced anorexia in chicks.
- To identify specific brain regions and neuropeptides involved in SP's appetite-suppressing effects.
Main Methods:
- Intracerebroventricular (ICV) injections of SP were administered to chicks.
- Diencephalon and hypothalamus tissues were isolated for mRNA expression analysis of key appetite-regulating neuropeptides and receptors.
- c-Fos immunoreactivity was quantified in hypothalamic nuclei to identify activated brain regions.
- mRNA expression was specifically analyzed in the paraventricular nucleus (PVN) following SP injection.
Main Results:
- SP administration dose-dependently reduced food intake in chicks without affecting water intake.
- SP did not alter the mRNA expression of neuropeptide Y (NPY), corticotropin-releasing factor (CRF), urocortin 3 (UCN 3), or their receptors in the diencephalon or hypothalamus.
- SP injection led to increased c-Fos immunoreactivity in the paraventricular nucleus (PVN), indicating its activation.
- In the PVN, SP increased urotensin 2 (UTS2) mRNA expression, while CRF and UCN3 mRNA levels remained unchanged.
Conclusions:
- SP-induced anorexia in chicks is mediated by the activation of the paraventricular nucleus (PVN).
- The anorexigenic effects of SP may involve the upregulation of UTS2 within the PVN.
Abstract:
Exogenous administration of substance P (SP) exerts anorexigenic effects in both chicks and rats, but the central mechanism mediating this response is poorly understood. Therefore, this study was designed to elucidate mechanisms of SP-induced anorexia using chicks as models. Chicks that received intracerebroventricular (ICV) injections of SP dose-dependably reduced their food intake with no effect on water intake. Next, the diencephalon was isolated from SP-injected chicks and mRNA expression of neuropeptide Y (NPY), corticotropin releasing factor (CRF), urocortin 3 (UCN 3) and CRF receptors were measured but were not affected. When measured in the hypothalamus, mRNA abundance of these and NPY receptors, urotensin 2 (UTS2) and melanocortin receptor 4 (MCR4) were not affected by SP-injection. Quantification of c-Fos immunoreactivity in appetite-associated hypothalamic nuclei demonstrated that the paraventricular nucleus (PVN) was activated in SP-injected chicks. Finally, in the PVN isolated from SP-injected chicks, there was increased expression of UTS2 mRNA while CRF and UCN3 were not affected. Thus, the anorexigenic effects of SP appear to be mediated by PVN activation and may involve UTS2.
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