The release of [3H]monoamines from preloaded synaptosomes from spinal cord is K+-dependent and can be modulated by L-type Ca2+ channel agonists such as the 1,4-dihydropyridine (1,4-DHP), Bay K 8644. Whereas the basal release of [3H]monoamines was not altered by Bay K 8644, K+-stimulated release of [3H]norepinephrine was enhanced 35% and [3H]serotonin 50%. Modulation of release by Bay K 8644 was dependent on the K+ concentration in the medium, being present only at submaximal depolarization with 15 mM K+. Enhanced release in the presence of Bay K 8644 was concentration-dependent and Ca2+-dependent. Ca2+-independent release induced by fenfluramine was not enhanced by Bay K 8644. Both nimodipine and nitrendipine, 1,4-DHP antagonists, produced a concentration-dependent block of the Bay K 8644-induced monoamine release and had no independent effect on basal or K+-stimulated release. ω-Conotoxin GVIA (ω-CgTx) produced a concentration dependent decrease of K+-stimulated serotonin release, which antagonized the stimulatory effect of low concentrations of Bay K 8644. However, ω-CgTx did not alter the enhancement of K+-stimulated release at higher concentrations of Bay K 8644. The data from the present work establish the conditions for modulation of K+-evoked monoamine release in spinal cord by 1,4-DHP agonists and suggest a role for the L-type voltage dependent Ca2+ channel in this process.
- 5-HT release
- Ca channels (voltage-dependent)
- Spinal cord
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