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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.
Abstract:
The relative roles of dopaminergic and beta-adrenergic receptors in mediating the stress-induced increase in the secretion of alpha-melanocyte-stimulating hormone (alpha-MSH) from the intermediate lobe of the pituitary were determined in the male rat. Thirty minutes of physical immobilization (restraint stress) increased the circulating concentrations of alpha-MSH and decreased the 3,4-dihydroxyphenylacetic acid/dopamine (DOPAC/DA) ratio in the intermediate lobe of the pituitary, reflecting a decrease in the tuberohypophysial dopaminergic neuronal activity. Pretreatment with the beta-adrenergic antagonist propranolol reduced the stress-induced increase in the circulating levels of alpha-MSH, but had no effect on the basal plasma concentrations of this hormone or the stress-induced decrease in DOPAC/DA in the intermediate lobe. If the dopaminergic tone during stress was maintained by administration of the DA agonist apomorphine, the stress-induced increase in alpha-MSH secretion was prevented. In nonstressed animals the administration of the beta 2-adrenergic agonist metaproterenol increased the plasma levels of alpha-MSH, and the effect of this drug was augmented if the inhibitory dopaminergic tone on alpha-MSH secretion was blocked by the administration of the DA antagonist haloperidol. Severing neurons in the retrochiasmatic region of the hypothalamus blocked the stress-induced decrease in DOPAC/DA in the intermediate lobe and attenuated the stress-induced increase in plasma concentrations of alpha-MSH. Taken together, these results indicate that a decrease in tuberohypophysial dopaminergic neuronal inhibitory tone and an increase in beta-adrenergic stimulation are both necessary for the full expression of the stress-induced increase in secretion of alpha-MSH from melanotrophs in the intermediate lobe of the rat pituitary.
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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