Cellular distribution of β-endorphin-like substance in the rat pituitary and brain

Salih, H.; Panerai, Alberto E.; Friesen, Henry G.

doi:10.1016/0024-3205(79)90381-3

Cited by 24 publications

(4 citation statements)

References 11 publications

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“…The parallel increase of the three parameters seems to be the result of pituitary stimulation. It is known that the pituitary has a high content of 0-endorphin (Goldstein 1976) and that it is secreted by the same pituitary cells as ACTH (Salih, Panerai and Friesen 1979) from a common precursor, proopiocortin (Nakanishi, Inoue, Kita, Nakamura, Chang, Cohen and Numa 1979). The response of ACTH, /3-endorphin and Cortisol to calcitonin observed in the present study is similar to the response observed after corticotropin releasing factor (CRF) administration (Jackson, DeCherney, DeBold, Sheldon, Alexander and Rivier 1984;Hermus, Pieters, Smals, Benraad and Kloppenborg 1984).…”

Section: Discussionsupporting

confidence: 83%

Calcitonin Induced Increase in ACTH, β-Endorphin and Cortisol Secretion

Laurian¹,

Oberman²,

Graf³

et al. 1986

Horm Metab Res

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The response of ACTH, beta-endorphin and cortisol to calcitonin administration was investigated in 8 subjects with recent fractures of the vertebrae due to postmenopausal or senile osteoporosis (Ost) and in seven normal healthy controls (NC). A significant increase of the three hormones was observed in 13 subjects. The maximum increase was observed between 15 and 60 min.: the cortisol level (microgram/100 ml) rose from 14.3 +/- 1.9 to 24.8 +/- 3.2 (P less than 0.05) in Ost and from 7.7 +/- 0.6 to 21.7 +/- 1.7 (P less than 0.001) in NC, the beta-endorphin (pmol/l) from 5.8 +/- 0.6 and to 21.2 +/- 1.3 in OST (P less than 0.001) and from 5.9 +/- 0.4 to 21.9 +/- 4.5 (P less than 0.01) in NC and the ACTH levels (pg/ml) from 21.3 +/- 5.7 to 61.7 +/- 3.6 (P less than 0.001) in OST and from 30.0 +/- 6.2 to 58.8 +/- 7.5 (P less than 0.05) in NC. The results indicate a possible role of calcitonin in modulating the anterior pituitary function. It also suggests that the analgesic effect of calcitonin might be mediated by the increase of beta-endorphin. The possibility that this analgesic effect of calcitonin is due to its direct binding to the opiate receptors was excluded in the present study by in vitro binding assay.

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Section: Discussionsupporting

confidence: 83%

Calcitonin Induced Increase in ACTH, β-Endorphin and Cortisol Secretion

Laurian¹,

Oberman²,

Graf³

et al. 1986

Horm Metab Res

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“…acetylcholine and opiate binding sites (Creese et al, 1977;Schaeffer and Hsueh. 1980) and neuropeptides (Blackwell and Guillemin, 1973;Salih et al, 1979). Tissues with such intimate connections to nerve tissue may possess some similar biochemical features related to neural communication.…”

Section: Discussionmentioning

confidence: 99%

Neurotransmitter-related features of the retinal pigment epithelium

Bondy

Ali

Hong

et al. 1983

Neurochemistry International

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“…In addition, other ACTH-related peptides, including a-MSH and [1-endorphin, which are derived from the same common precursor molecule as ACTH, have been identified in cell bodies in the dorsal hy pothalamus [6,[20][21][22] and in a number of extrahypothalamic sites including the amygdala and brain stem [5,19]. Fur thermore, other evidence has suggested that ACTH and its related peptides originate in sites outside the ventral hypo thalamus.…”

Section: Discussionmentioning

confidence: 99%

Origin of Immunoreactive ACTH in Brain Sites Outside the Ventral Hypothalamus

Kapcala¹,

Lechan²,

Reichlin³

1983

Neuroendocrinology

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Immunoreactive adrenocorticotropin (IR-ACTH) is widely distributed throughout the brain. Highest concentrations have been localized in the ventral hypothalamus, a recognized site of origin of IR-ACTH containing neuronal cell bodies. To determine whether IR-ACTH arises in other brain sites, we determined the effect on the concentration of IR-ACTH in several regions of rat brain after intracerebroventricular injection of colchicine, an agent that inhibits axoplasmic transport and leads to an accumulation of neuronal secretory products within cell bodies. Three regions (ventral hypothalamus, dorsal hypothalamus, amygdala) showed a significant increase in concentration of IR-ACTH after colchicine, whereas the hippocampus and preoptic area did not. Because neuropeptides, in general, undergo posttranslational processing during axoplasmic transport, it could be predicted that inhibition of transport would lead to a relative increase in ‘large’, precursor forms of hormone in regions containing cells of origin of neuropeptide tracts. Therefore, the effect of colchicine on the processing of molecular forms of IR-ACTH was also examined. In brain regions showing a significant increase in IR-ACTH after colchicine, the proportion of ’big’ ACTH and ACTH_1–39 (relative to total IR-ACTH) increased and the proportion of ‘small’ ACTH (<4,500 daltons) declined. In contrast, size distribution of IR-ACTH species in other areas were either the opposite or were unchanged. These studies indicate that in addition to the ventral hypothalamus, IR-ACTH also originates in the dorsal hypothalamus and the amygdala, and that decreased axoplasmic peptide transport is associated with decreased processing of molecular forms.

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Cellular distribution of β-endorphin-like substance in the rat pituitary and brain

Cited by 24 publications

References 11 publications

Calcitonin Induced Increase in ACTH, β-Endorphin and Cortisol Secretion

Calcitonin Induced Increase in ACTH, β-Endorphin and Cortisol Secretion

Neurotransmitter-related features of the retinal pigment epithelium

Origin of Immunoreactive ACTH in Brain Sites Outside the Ventral Hypothalamus

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