Potassium-induced secretion of melanocyte-stimulating hormone from the melanotrophs of the neurointermediate lobe of the lizard Anolis carolinensis.
Secretion of melanocyte-stimulating hormone (MSH) from the melanotrophs of the neurointermediate lobe (NIL) of the lizard Anolis carolinensis was studied to investigate the role of membrane potential and extracellular calcium ions in the control of secretion in this species. MSH secretion was monitored from perifused NILs which had been in organ culture for 7-14 days prior to experiment to allow the nerve terminals present in the tissue to degenerate. Elevation of the K(+) concentration in the perifusate induced a marked increase in MSH secretion. Perifusion of the cultured NILs with a nominally Ca-free solution did not reduce basal MSH secretion but blocked K-induced secretion. Moreover, nimodipine, an antagonist of voltage-gated Ca(2+) channels, inhibited K-induced secretion, whereas BAY K 8644, a Ca(2+) channel agonist, potentiated it; but neither drug affected basal secretion. High ¿K(+) perifusate also stimulated MSH secretion from freshly excised (acute) NILs. Furthermore, in these preparations nominally Ca-free solution reduced basal secretion by 40% in addition to blocking K-induced secretion. As in the cultured NILs, nimodipine blocked and BAY K 8644 potentiated K-induced secretion in the acute NILs while not affecting basal secretion. The results from the cultured NILs are consistent with the hypothesis that stimulated MSH secretion from the melanotrophs of the anole is dependent upon Ca(2+) influx through voltage-gated calcium channels. The qualitatively similar results obtained from the acute NILs in response to high ¿K(+), nimodipine, and BAY K 8644 suggest that, for the most part, what is being observed are the direct effects of these substances on the melanotrophs. Basal secretion of MSH in cultured NILs is significantly less than that in the acute preparations. The calcium-sensitive fraction of basal secretion present in acute NILs may require the presence of nerve terminals.
Lyons
H J
HJ
College of Liberal Arts, Florida Atlantic University, Davie, Florida 33314, USA.
Lyons
L F
LF
Taraskevich
P S
PS
D001498:3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester / Q000494:pharmacology; D000818:Animals; D002118:Calcium / Q000494:pharmacology; D002120:Calcium Channel Agonists / Q000494:pharmacology; D002121:Calcium Channel Blockers / Q000494:pharmacology; D015220:Calcium Channels / Q000187:drug effects / Q000502:physiology; D002478:Cells, Cultured; D008116:Lizards / Q000502:physiology*; D009074:Melanocyte-Stimulating Hormones / Q000096:biosynthesis* / Q000378:metabolism*; D009553:Nimodipine / Q000494:pharmacology; D010902:Pituitary Gland / Q000187:drug effects* / Q000378:metabolism*; D011188:Potassium / Q000494:pharmacology*
D002120:Calcium Channel Agonists; D002121:Calcium Channel Blockers; D015220:Calcium Channels; D009553:Nimodipine; D001498:3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester; D009074:Melanocyte-Stimulating Hormones; D011188:Potassium; D002118:Calcium