| Summary: | 碩士 === 東吳大學 === 微生物學系 === 89 === Abstract
Effects of amphetamine on calcium fluxes and secretion in bovine adrenal chromaffin cells and PC12 cells were investigated. Amphetamine induced a calcium rise ( by itself ) and blocked the 1,1-Dimethyl -4-phenyl -piperazinium iodide (DMPP) -induced [Ca2+]i rise, yet have very little effects on the high K+-induced [Ca2+]i rise in bovine chromaffin cells. Nomifensine, a Norepinephrine transporter (NET) inhibitor, suppressed both DMPP- and high K+-induced [Ca2+]I rise. We suggest that amphetamine and nomifensine addressed different effects on stimulation coupled calcium signal in bovine cells, the blockage of nomifensine was through its blockage of voltage -sensitive calcium channels yet it is not the case of amphetamine. In PC12 cells, amphetamine, GBR12909 and nomifensine all blocked the ATP- and high K+-induced [Ca2+]i rise. We suggest they all share some similar chemistry character, thus to suppress stimulation coupled calcium signals in PC12 cells by a similar pathway-- voltage-sensitive calcium channels. Since P2Y coupled calcium signals cannot be measured in a calcium free buffer, we suggest that the partially blockage effects of amphetamine is mainly on P2X purinoceptors. Interestingly, chronic treatment of either DMPP or amphetamine successfully promoted the function of nicotinic receptors, yet with little influence to P2 purinoceptors. We conclude that amphetamine address different effects on nicotinic receptors and P2X purinoceptors.
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