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• W2149671406 abstract "1 The ability of calcimycin, cyclopiazonic acid and thapsigargin to facilitate the N-methyl-D-aspartate (NMDA)-mediated depolarization of cortical projection neurones was investigated by use of grease-gap recording and the results compared with the facilitation that results from activation of 5-hydroxytryptamine2A receptors. 2 Calcimycin (0.25 to 3 μm), cyclopiazonic acid (5 to 30 μm), and thapsigargin (10 to 300 nM) reversibly facilitated the NMDA (50 μm)-induced depolarization in the presence of tetrodotoxin. The concentration-response relationships were bell-shaped with a mean enhancement of 550% for calcimycin (1 μm) and approximately 400% for cyclopiazonic acid (20 μm) and thapsigargin (100 nM). At the highest concentration of each agent tested, no facilitation was observed. 3 Chlorpromazine (1 μm) partially restored a facilitation at 3 μm calcimycin and 300 nM thapsigargin. Myo-inositol (10 mM) and 100 nM staurosporine were both ineffective in this regard. 4 The depolarization elicited by 10 μm quisqualate or 5 μm kainate was not facilitated by 10 μm cyclopiazonic acid. 5 Calcimycin (0.5 μm), cyclopiazonic acid (20 μm), and thapsigargin (100 nM) elicited a significant facilitation in the presence of an antagonist cocktail consisting of D, L-2-amino-3-phosphonopropionic acid, prazosin, ritanserin, and scopolamine, although the magnitude of the facilitation was reduced. 6 Facilitation of the NMDA depolarization elicited by both 30 μm 5-hydroxytryptamine and 10 μm phenylephrine was eliminated in nominally Mg2+-free medium. In contrast, the facilitation induced by 0.5 μm calcimycin remained intact. 7 Bis-(o-aminophenoxy)-ethane-N,N,N,N, tetraacetic acid aminoethoxy (50 μm) or perfusion with nominally Ca2+-free medium eliminated facilitation of the NMDA depolarization induced by 30 μm 5-hydroxytryptamine and 100 nM thapsigargin. 8 The facilitation induced by both 30 μm 5-hydroxytryptamine and 1 μm calcimycin was reduced in a concentration-dependent manner by nifedipine (1 to 10 μm). 9 Calcimycin, cyclopiazonic acid and thapsigargin facilitate the NMDA depolarization in a manner which closely mimics the facilitation induced by 5-hydroxytryptamine. It is concluded that enhancement of the NMDA depolarization at cortical projection neurones results from an elevation of Ca2+ in the cytosol and that several sources of Ca2+ contribute to the facilitation." @default.
• W2149671406 created "2016-06-24" @default.
• W2149671406 creator A5002550841 @default.
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• W2149671406 date "1996-11-01" @default.
• W2149671406 modified "2023-09-29" @default.
• W2149671406 title "Action of 5-hydroxytryptamine in facilitating N-methyl-D-aspartate depolarization of cortical neurones mimicked by calcimycin, cyclopiazonic acid and thapsigargin" @default.
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• W2149671406 doi "https://doi.org/10.1111/j.1476-5381.1996.tb15754.x" @default.
• W2149671406 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/1915930" @default.
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