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• W2001253680 abstract "The dipeptide carnosine (beta-alanyl-L-histidine) has been proposed as a neurotransmitter in the mammalian olfactory pathway. Therefore, the efflux of in vivo-synthesized [14C]carnosine from mouse olfactory bulb synaptosomes was investigated. Carnosine was found to be released from the olfactory bulb synaptosomes by two mechanisms. The first is a slow spontaneous process that is independent of depolarization. The rate of this release was doubled in the presence of 1 mM external carnosine. Release by the second mechanism was markedly stimulated in the presence of calcium by depolarization with either 60 mM K+ or 300 microM veratridine. Omission of calcium abolished the stimulatory effect of both of these agents. Further, blockage of the veratridine-induced depolarization by tetrodotoxin also inhibited carnosine release. These results are consistent with the hypothesis that carnosine acts as a neurotransmitter in the mouse olfactory pathway." @default.
• W2001253680 created "2016-06-24" @default.
• W2001253680 creator A5036478606 @default.
• W2001253680 creator A5078097800 @default.
• W2001253680 date "1982-06-01" @default.
• W2001253680 modified "2023-09-29" @default.
• W2001253680 title "Carnosine Release from Olfactory Bulb Synaptosomes Is Calcium-Dependent and Depolarization-Stimulated" @default.
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• W2001253680 doi "https://doi.org/10.1111/j.1471-4159.1982.tb06626.x" @default.
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