Rochel S, Margolis F L
J Neurochem. 1982 Jun;38(6):1505-14. doi: 10.1111/j.1471-4159.1982.tb06626.x.
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.
二肽肌肽（β-丙氨酰-L-组氨酸）被认为是哺乳动物嗅觉通路中的一种神经递质。因此，研究了体内合成的[14C]肌肽从小鼠嗅球突触体中的流出情况。发现肌肽通过两种机制从嗅球突触体中释放出来。第一种是缓慢的自发过程，与去极化无关。在存在1 mM外部肌肽的情况下，这种释放速率增加了一倍。第二种机制的释放受到钙的显著刺激，通过用60 mM K+或300 microM藜芦碱进行去极化。去除钙消除了这两种试剂的刺激作用。此外，河豚毒素对藜芦碱诱导的去极化的阻断也抑制了肌肽的释放。这些结果与肌肽在小鼠嗅觉通路中作为神经递质起作用的假设一致。
