Polyamine potentiation and inhibition of NMDA-mediated increases of intracellular free Ca2+ in cultured chick cortical neurons.
Abstract
Polyamine potentiation and inhibition of (NMDA) receptor-mediated CA2+ changes was studied in cultured chick cortical neurons. Spermidine and spermine potentiated the effect of saturating concentrations of NMDA and glycine. No effect of spermidine or spermine was observed in the absence of NMDA or in the presence of either kainate or quisqualate. Similarly, antagonism of the NMDA receptor complex with dizocilpine (an open channel blocker), or with competitive antagonists to the NMDA or glycine binding sites greatly attenuated or completely abolished the combined effects of polyamines plus NMDA and glycine. N-Acetylspermine and N-acetylspermidine, in the presence or absence of NMDA and glycine, were without effect. These data strongly suggest that spermidine and spermine are potent and selective agonists at the polyamine binding site. Putrescine and diethylenetriamine were ineffective as antagonists of NMDA-mediated intracellular free Ca2+ increases in the presence or absence of added spermine or spermidine. Arcaine and 1,10-diaminodecane, however, antagonized NMDA-mediated intracellular free Ca2+ increases in the presence and absence of spermine and spermidine, and therefore appear to act either as inverse agonists at the polyamine binding site or as open channel blockers of the NMDA receptor.
Department
Biological Sciences
Publication Date
1-15-1994
Journal Title
European journal of pharmacology
Publisher
Elsevier
Digital Object Identifier (DOI)
Document Type
Article
Recommended Citation
Gary A. Pritchard, Jeanne M. Fahey, Subhash C. Minocha, Cathleen Conaty, Lawrence G. Miller, Polyamine potentiation and inhibition of NMDA-mediated increases of intracellular free Ca2+ in cultured chick cortical neurons, European Journal of Pharmacology: Molecular Pharmacology, Volume 266, Issue 2, 1994, Pages 107-115, ISSN 0922-4106, https://doi.org/10.1016/0922-4106(94)90099-X.
Rights
Copyright © 1994 Published by Elsevier B.V.