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Related Experiment Videos

Nicotine elevates rat plasma ACTH by a central mechanism.

S G Matta1, H S Beyer, K M McAllen

  • 1Minneapolis Medical Research Foundation, Minnesota.

The Journal of Pharmacology and Experimental Therapeutics
|October 1, 1987
PubMed
Summary

Nicotine stimulates adrenocorticotropin (ACTH) release by acting on the central nervous system, specifically the hypothalamus or brainstem. This effect is observed in rats from early postnatal development, indicating a central mechanism for nicotine-induced ACTH secretion.

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Area of Science:

  • Neuroendocrinology
  • Pharmacology
  • Physiology

Background:

  • Nicotine is known to stimulate adrenocorticotropin (ACTH) release in vivo.
  • The precise site of nicotine's action in mediating ACTH release remains undetermined.
  • Understanding the mechanism is crucial for elucidating nicotine's physiological effects.

Purpose of the Study:

  • To investigate the central versus peripheral site of nicotine's action on ACTH release.
  • To determine the developmental timeline of nicotine's effect on ACTH secretion.
  • To elucidate the neural pathways involved in nicotine-induced ACTH release.

Main Methods:

  • Administration of nicotine and cytisine (peripherally acting agonist) intravenously.
  • In vitro studies on anterior pituicytes to assess direct pituitary effects.

Related Experiment Videos

  • Intracerebroventricular and intra-hypothalamic injections of nicotine.
  • Assessment of ACTH levels following administration of nicotinic antagonists (hexamethonium and mecamylamine).
  • Evaluation of nicotine's effect on ACTH release during the postnatal developmental period.

    • Main Results:

    • Peripherally administered cytisine did not elevate plasma ACTH, unlike nicotine.
    • Nicotine did not directly affect beta-endorphin secretion from pituicytes in vitro or potentiate CRF action.
    • Intracerebroventricular nicotine significantly increased ACTH levels, with greater effect when delivered to the hypothalamus.
    • Nicotine-induced ACTH release was present but diminished in early postnatal rats, reaching adult levels by day 15.
    • The centrally acting antagonist mecamylamine blocked nicotine-induced ACTH release, while the peripheral antagonist hexamethonium was ineffective.

    Conclusions:

    • Nicotine stimulates ACTH release through central mechanisms, likely acting within the hypothalamus or brainstem.
    • The effect of nicotine on ACTH release is developmentally regulated, with significant responses emerging by day 15 postnatally.
    • These findings highlight the central neural targets mediating nicotine's potent secretagogue action on ACTH.