HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text (PDF) Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Valentijn, J A Articles by Cazin, L Search for Related Content PubMed PubMed Citation Articles by Valentijn, J A Articles by Cazin, L

European Institute for Peptide Research, Laboratory of Molecular Endocrinology, CNRS URA 650, UA INSERM, University of Rouen, Mont-Saint-Aignan, France.

1. Melanostatin, a thirty-six amino acid peptide recently isolated from the frog brain due to its ability to inhibit alpha-melanocyte-stimulating hormone (alpha-MSH) release, is the amphibian counterpart of mammalian neuropeptide Y (NPY). The effect of synthetic melanostatin on the bioelectrical activity of cultured frog melanotrophs was studied in 124 cells by using the whole-cell patch-clamp technique. 2. In current-clamp experiments, melanostatin (1 microM) provoked a reversible hyperpolarization and a suppression of spontaneous action potentials. In some cells the hyperpolarizing response was absent, but an arrest of spike firing still occurred. 3. Melanostatin-induced hyperpolarization was associated with a decrease in membrane resistance. In voltage-clamp experiments, melanostatin induced an outward current at a constant command potential. This hyperpolarizing outward current appeared to be carried by potassium ions. 4. Cell dialysis with the non-hydrolysable GTP analogue guanosine-5'-O-(3-thiotriphosphate) (GTP gamma S) sustained the outward current produced by melanostatin. Dopamine (1 microM), which generates a similar hyperpolarizing outward current in frog melanotrophs, was not capable of increasing the current provoked by melanostatin and sustained by GTP gamma S. 5. Melanostatin also modulated voltage-operated currents. The amplitude of voltage-activated potassium current was increased by 30%. 6. Melanostatin reduced the fast sodium current. This inhibitory effect was rather persistent compared to the other modulated currents. 7. Melanostatin markedly scaled down high voltage-activated N- and L-like calcium currents. The activation kinetics of these two calcium currents were not altered by the peptide. 8. Pretreatment of melanotrophs with pertussis toxin (1 microgram ml-1) blocked melanostatin-induced inhibition of N- and L-like calcium currents. 9. It is concluded that the NPY-related peptide melanostatin generates a very complex pattern of electrical responses in frog melanotrophs, including hyperpolarization and modulation of voltage-activated currents underlying action potentials. G proteins appear to mediate at least part of these effects.

This article has been cited by other articles:

				L. Galas, M.-C. Tonon, D. Beaujean, R. Fredriksson, D. Larhammar, I. Lihrmann, S. Jegou, A. Fournier, N. Chartrel, and H. Vaudry Neuropeptide Y Inhibits Spontaneous {alpha}-Melanocyte-Stimulating Hormone ({alpha}-MSH) Release via a Y5 Receptor and Suppresses Thyrotropin-Releasing Hormone-Induced {alpha}-MSH Secretion via a Y1 Receptor in Frog Melanotrope Cells Endocrinology, May 1, 2002; 143(5): 1686 - 1694. [Abstract] [Full Text] [PDF]

				O. Soriani, F. L. Foll, F. Roman, F. P. Monnet, H. Vaudry, and L. Cazin A-Current Down-Modulated by sigma  Receptor in Frog Pituitary Melanotrope Cells Through a G Protein-Dependent Pathway J. Pharmacol. Exp. Ther., April 1, 1999; 289(1): 321 - 328. [Abstract] [Full Text]