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.

Neuropeptides
|July 10, 2014
PubMed

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.

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