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Biomedical subjects

M E Hadley

Publications and source records attributed to M E Hadley.

At least 127 records · Page 7Linked to original sources
PubMed1978

Pars intermedia electrical potentials: changes in spike frequency induced by regulatory factors of melanocyte stimulating hormone (MSH) secretion.

Spontaneous action potentials recorded from pars intermedia (PI) cells of frog pituitaries are correlated with spontaneous melanophore stimulating hormone (MSH) secretion from that gland. Those agents known to induce hormone release (e.g., serotonin, isoproterenol) increase the rate of electrical activity, whereas those which inhibit secretion (e.g., norepinephrine, dopamine, GABA) reduce the frequency of spikes. MSH secretion appears to involve cellular depolarization while inhibition of release is associated with cell membrane polarization.

Action Potentials↗
PubMed1976

Ergot alkaloid inhibition of melanophore stimulating hormone secretion.

Ergonovine maleate inhibits melanophore stimulating hormone (MSH) secretion from the incubated frog, rat, and mouse pituitary gland. This ergot alkaloid is partially effective at a concentration as low as 10(-8)M. The inhibitory effect on hormone release is irreversible under the experimental conditions studied. Ergonovine inhibition of MSH secretion is blocked by Dibenamine and chlorpromazine as is dopamine inhibition of MSH secretion. At higher concentrations chlorpromazine as is dopamine inhibition of MSH secretion. Similarities between the cellular mechanisms controlling MSH and prolactin secretion will be discussed.

Animals↗
PubMed1975

Melanophore stimulating hormone (MSH) release: inhibition by cytochalasin B and "stimulation" by dimethyl sulfoxide.

Incubation of rat or frog pituitaries in cytochalasin B (10-4 minus 10-8 g/ml) for 2, 4 or 6 hr produces a time-dependent inhibition of MSH release. This inhibition is reversible and, again, time-dependent since longer incubations of pituitaries returned to normal media result in greater hormone secretion. Cytochalasin B inhibits MSH release even at a high concentration (10%) of dimethylsulfoxide (DMSO) which, itself, is "stimulatory" to hormone release. MSH release in high DMSO concentration is also inhibited by ouabain or by the absence of Ca2+ from the medium. In amphibian Ringer enriched with glucose, and in Medium 199, cytochalasin B fails to inhibit the release of MSH from the frog pituitary. Colchicine, vinblastine, and vincristine (10-3 minus 10-6 g/ml) were without effect on MSH release. These data suggest a possible role for microfilaments in the control of MSH release but fail to provide information on the exact nature of the mechanisms involved.

Animals↗
PubMed1974

Biogenic amines and control of melanophore stimulating hormone release.

Release of melanophore stimulating hormone (MSH) from the vertebrate pars intermedia is under inhibitory control by the hypothalamus. Removal of the rat pituitary or the neurointermediate lobe of the frog (Rana pipiens) to in vitro incubation medium results in rapid uninhibited release of MSH. This secretion is inhibited by norepinephrine, epinephrine, phenylephrine, and dopamine, and the inhibition is antagonized by alpha-adrenergic receptor blocking agents. Isoproterenol stimulation of MSH secretion from isolated glands is blocked by pro-pranolol, a beta-adrenergic receptor antagonist. These results implicate dopaminergic or classical alpha-adrenergic receptors (or both) in inhibition of MSH release by catecholamines, and implicate beta-adrenergic receptors in stimulation of MSH release by the bioamines.

Animals↗
PubMed1972

Melanophore stimulating hormone: release inhibition by ring structures of neurohypophysial hormones.

Tocinamide and tocinoic acid, ring structures of oxytocin, are potent inhibitors of the release of melanophore stimulating hormone from the rat and hamster pituitary in vitro. Tocinamide is effective at concentrations as low as 10-(14)M on the mammalian pituitary. These peptides do not affect release of the hormone on the frog (Rana pipiens) pars intermedia, but they do inhibit release in the bullfrog (Rana catesbeiana) and the toad (Bufo marinus). The specificity of the peptides on inhibition of the hormone is demonstrated by the fact that oxytocin, lysine vasopressin, and pressinoic acid and pressinamide (ring structures of the vasopressins) do not show such inhibitory activity. Hypothalamic extracts of either the frog (Rana pipiens) or the rat inhibit release of the hormone from pituitaries of either species. The inhibitory effects of tocinamide and tocinoic acid, like that of hypothalamic extracts, are reversible.

Animals↗