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Clonidine hyperphagia: neuroanatomic substrates and specific function.

G Shor-Posner1, A P Azar, M Volpe

  • 1Rockefeller University, New York, NY 10021.

Pharmacology, Biochemistry, and Behavior
|August 1, 1988
PubMed
Summary
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The alpha 2-noradrenergic agonist clonidine (CLON) stimulates feeding and carbohydrate preference in rats, acting on postsynaptic alpha 2 receptors in the hypothalamic paraventricular nucleus (PVN). This suggests the PVN is key for CLON-induced hyperphagia.

Area of Science:

  • Neuroscience
  • Neuropharmacology
  • Behavioral Neuroscience

Background:

  • Alpha 2-noradrenergic agonists like clonidine (CLON) can stimulate feeding, similar to norepinephrine (NE).
  • Previous studies suggest the hypothalamic paraventricular nucleus (PVN) is involved in NE-stimulated feeding.

Purpose of the Study:

  • To investigate the effects of clonidine on meal patterns and macronutrient selection.
  • To compare clonidine's feeding effects with those of norepinephrine.
  • To determine the role of the PVN in clonidine-induced feeding.

Main Methods:

  • Administered clonidine directly into the PVN and peripherally in rats.
  • Utilized PVN electrolytic and 6-hydroxydopamine lesions to study clonidine's effects.
  • Assessed changes in meal size, feeding duration, meal frequency, and food intake, with a focus on macronutrient selection (carbohydrates).

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Main Results:

  • Direct PVN administration of clonidine increased meal size and feeding duration, mimicking NE.
  • Peripheral clonidine administration increased food intake and specifically potentiated carbohydrate ingestion in sham-operated rats.
  • PVN electrolytic lesions abolished clonidine-induced feeding and carbohydrate preference, while 6-hydroxydopamine lesions did not affect it.

Conclusions:

  • The PVN appears to be a primary site for clonidine-stimulated hyperphagia.
  • Clonidine likely acts on postsynaptic alpha 2 receptors within the PVN to enhance carbohydrate intake.
  • This mechanism may involve direct receptor activation rather than presynaptic norepinephrine release.