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Carnosine Release from Olfactory Bulb Synaptosomes Is Calcium‐Dependent and Depolarization‐Stimulated
Author(s) -
Rochel S.,
Margolis F. L.
Publication year - 1982
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.1982.tb06626.x
Subject(s) - olfactory bulb , carnosine , depolarization , chemistry , synaptosome , calcium , biophysics , neuroscience , biochemistry , biology , central nervous system , organic chemistry
The dipeptide carnosine (β‐alanyl‐L‐histidine) has been proposed as a neurotransmitter in the mammalian olfactory pathway. Therefore, the efflux of in vivo ‐synthesized [ 14 C]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 m M external carnosine. Release by the second mechanism was markedly stimulated in the presence of calcium by depolarization with either 60 m M K + or 300 μ M 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.