Stress-Induced Secretion of Pro-Opiomelanocortin-Derived Peptides in Rats: Relative Importance of the Anterior and Intermediate Pituitary Lobes

Abstract

Stress stimulates secretion of the pro-opiomelanocortin (POMC)-derived peptides adrenocorticotropic hormone (ACTH), β-endorphin (β-END) and α-melanocyte-stimulating hormone (α-MSH) from the anterior lobe (AL) and intermediate lobe (IL) of the pituitary gland. The secretion of POMC-derived peptides from the AL and IL is differentially regulated and the relative contribution of the lobes may vary with the stimulus. We investigated (1) the relative importance of the AL and IL as source of POMC-derived peptides released in response to restraint and ether stress by selectively inhibiting the corticotropes of the AL by dexamethasone (DEX) or selectively inhibiting the melanotropes of the IL by bromocriptine (BR), and (2) whether β-adrenergic blockade by propranolol could be used to discriminate between the stress-induced effect on POMC secretion from the AL and IL as has previously been suggested. Selective inhibition of AL secretion by DEX totally blocked the ACTH response to restraint and ether stress, but only partially inhibited the β-END response. The α-MSH response to both stressors was not affected by DEX. Conversely, selective inhibition of IL secretion by BR totally blocked the α-MSH response to both stressors, partially inhibited the β-END response but did not influence the ACTH response. In response to restraint stress, β-END was secreted equally from the AL and IL, whereas the IL was the most important source of β-END in response to ether stress. Blockade of β-adrenergic receptors with propranolol inhibited the β-END- and α-MSH responses to restraint stress whereas the ACTH response was unaffected. The secretory response of both ACTH, β-END and α-MSH to ether stress was inhibited by propranolol. We conclude, that (1) restraint- and ether-stress-induced secretion of ACTH and α-MSH are of AL and IL origin, respectively, (2) β-END secreted in response to restraint stress originates almost equally from the AL and IL, whereas the source of β-END in response to ether stress is mainly the IL, and (3) β-adrenergic blockade by propranolol cannot be used to discriminate between the AL and IL as the source of POMC peptides secreted in response to stress.

The Neuroendocrine Protein 7B2 Suppresses the Aggregation of Neurodegenerative Disease-related Proteins

“…Recombinant Aβ 1–42 and Aβ 1–40 were purchased from Biopeptide Co. (San Diego, CA), and α-synuclein was expressed and purified as described (30). Aβ 1–40 and Aβ 1–42 were diluted in 0.5% Me 2 SO and 0.5 m Tris-HCl buffer (pH 7.4; 1 mg/ml) and then diluted into 40 μ m ThT solutions (in quadruplicate) containing or lacking the various forms of 7B2 in a total volume of 100 μl.…”

Plasma α-MSH and acetylated β-endorphin levels following stress vary according to CRH sensitivity of the pituitary melanotropes in common carp, Cyprinus carpio

“…N-terminally acetylated -endorphin (NAc -end) and -melanocyte-stimulating hormone ( -MSH) are proopiomelanocortin (POMC)-derived peptide hormones produced and released by melanotrope cells in the pituitary pars intermedia. In many vertebrate classes, these hormones have been implicated in stress responses (Akil et al, 1985;Arends et al, 1999;Kjaer et al, 1995;Lindley et al, 1990;Lookingland et al, 1991;Mosconi et al, 1998;Wendelaar Bonga, 1997). In Mozambique tilapia (Oreochromis mossambicus), -MSH stimulates cortisol release from the interrenal cells in the head kidney (Lamers et al, 1992), and its corticotropic activity may be potentiated by NAc -end .…”

Dynamic Alterations in Growth Hormone Receptor mRNA Levels in Rat Brain During Stress Tolerance.

“…In addition to GHR mRNA, Somatostatin (SS) and GH-releasing factor (GRF) neurons are also detected in the arcuate (ARC), periventricular (PeV) and paraventricular nuclei of the rat [4]. Several laboratories have reported that various kinds of stress decrease the circulating level of GH in the rat [5][6][7]. This repressive effect of stress on GH secretion is proposed to occur via stress-induced hypothalamic corticotropin-releasing factor (CRF) stimulating the inhibitory somatostatin release into portal blood [7].…”