Dopaminergic and beta-adrenergic receptor control of alpha-melanocyte-stimulating hormone secretion during stress

S E Lindley1, K J Lookingland, K E Moore

  • 1Department of Pharmacology/Toxicology, Michigan State University, East Lansing.

Neuroendocrinology
|July 1, 1990
PubMed

Insights

Stress increases alpha-melanocyte-stimulating hormone (alpha-MSH) secretion via reduced dopaminergic activity and increased beta-adrenergic stimulation in the rat pituitary. Both pathways are essential for the full stress response.

Area of Science:

  • Neuroendocrinology
  • Adrenergic signaling
  • Dopaminergic signaling

Background:

  • Stress significantly impacts hormonal regulation.
  • The intermediate pituitary lobe secretes alpha-melanocyte-stimulating hormone (alpha-MSH).
  • Dopaminergic and adrenergic systems modulate alpha-MSH release.

Purpose of the Study:

  • To elucidate the roles of dopaminergic and beta-adrenergic receptors in stress-induced alpha-MSH secretion.
  • To investigate the neural pathways involved in this neuroendocrine response.

Main Methods:

  • Restraint stress applied to male rats.
  • Measurement of plasma alpha-MSH levels.
  • Analysis of 3,4-dihydroxyphenylacetic acid/dopamine (DOPAC/DA) ratio in the intermediate pituitary.
  • Pharmacological manipulation using receptor agonists and antagonists.
  • Surgical intervention (neuronal severing).

Main Results:

  • Stress decreased tuberohypophysial dopaminergic activity and increased circulating alpha-MSH.
  • Beta-adrenergic antagonism (propranolol) reduced stress-induced alpha-MSH increase.
  • Dopamine agonist (apomorphine) prevented stress-induced alpha-MSH secretion.
  • Beta 2-adrenergic agonist (metaproterenol) increased alpha-MSH, potentiated by dopamine antagonist (haloperidol).
  • Hypothalamic neuronal severing attenuated the stress response.

Conclusions:

  • Both reduced dopaminergic inhibition and enhanced beta-adrenergic stimulation are crucial for stress-induced alpha-MSH release.
  • The tuberohypophysial dopaminergic system and beta-adrenergic pathways interact to regulate alpha-MSH secretion under stress.

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