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首页> 外文期刊>Neurochemistry International: The International Journal for the Rapid Publication of Critical Reviews, Preliminary and Original Research Communications in Neurochemistry >Distinct temperature-dependent dopamine-releasing effect of drugs of abuse in the olfactory bulb.
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Distinct temperature-dependent dopamine-releasing effect of drugs of abuse in the olfactory bulb.

机译：嗅球中滥用药物具有明显的温度依赖性多巴胺释放作用。

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It was recently shown in the olfactory bulb (OB) that the response to olfactory stimulation might be related to local reinforcement mechanisms involved in discrimination of different odors. Therefore, it seemed interesting to study the effects of several drugs of abuse on the release of dopamine (DA) in the OB. Nicotine, amphetamine, 3,4-methylenedioxymethamphetamine (MDMA, "ecstasy"), and cocaine at 37 degrees C increased the release of [3H] DA from olfactory bulb slice preparations of the rats. While nicotine, amphetamine, and MDMA directly evoked DA release, cocaine, by inhibiting the reuptake processes, enhanced the electrical stimulation-evoked release. At low temperature (17 degrees C), a condition in which the transmitter uptake carriers of the plasma membrane in both the normal and reverse mode of operation are inhibited, the nicotine-evoked [3H] DA release was potentiated, whereas those evoked by amphetamine and MDMA were inhibited. At low temperature the field stimulation-evoked [3H] DA release was potentiated, but under this condition cocaine failed to increase the release. Our results show that low temperature (a) increases the concentration of extracellular DA released by Ca(2+)-dependent vesicular exocytosis elicited by nicotine, (b) inhibits the extracellular Ca(2+)-independent amphetamine- and MDMA-induced release of DA that occurs by the reverse operation of membrane carriers transporting DA from the cytoplasm of presynaptic terminals to the extraneuronal space, and (c) does not alter the inhibitory effect of cocaine on DA uptake that increases the concentration of extracellular DA released by field stimulation. The findings that the drugs of abuse tested all enhanced the release of DA in the olfactory bulb suggest that local reinforcing mechanisms may also exist in this brain area. In addition, we also show that lowering the temperature in in vitro experiments is an easy and straightforward method for separating vesicular and cytoplasmic release of transmitters, and is suitable for studying the mechanism of catecholamine release evoked by drugs of abuse. This technique may be applicable in other neurochemical studies that need inhibition of the uptake carriers without the blockade of the ligand-gated ion channels caused by reuptake inhibitor drugs.
机译：最近在嗅球（OB）中显示，对嗅觉刺激的反应可能与涉及区分不同气味的局部增强机制有关。因此，研究几种滥用药物对OB中多巴胺（DA）释放的影响似乎很有趣。尼古丁，苯丙胺，3,4-亚甲二氧基甲基苯丙胺（MDMA，“摇头丸”）和可卡因在37°C下可增加大鼠嗅球切片制剂中[3H] DA的释放。尼古丁，苯丙胺和摇头丸直接引起DA释放，而可卡因则通过抑制再摄取过程增强了电刺激引起的释放。在低温（17摄氏度）下，在正常和反向操作模式下质膜的递质摄取载体均被抑制的条件下，尼古丁诱发的[3H] DA释放被增强，而苯丙胺引起的释放和MDMA被抑制。在低温下，可引起场刺激的[3H] DA释放增强，但在这种情况下可卡因未能增加释放。我们的结果表明，低温（a）增加了尼古丁引起的Ca（2+）依赖性囊泡胞吐作用释放的细胞外DA的浓度，（b）抑制了细胞外Ca（2+）依赖性苯丙胺和MDMA诱导的释放通过膜载体将DA从突触前末端的胞质转运到神经外间隙而发生的DA的反向操作所产生的DA的变化;（c）不会改变可卡因对DA摄取的抑制作用，该抑制作用会增加通过电场刺激释放的细胞外DA的浓度。滥用药物进行测试的所有发现均增强了嗅球中DA的释放，表明该大脑区域也可能存在局部增强机制。此外，我们还表明，在体外实验中降低温度是分离递质的囊泡和细胞质释放的简便方法，并且适合研究滥用药物引起的儿茶酚胺释放机制。此技术可能适用于其他需要抑制摄取载体而又不会因再摄取抑制剂药物引起的配体门控离子通道受阻的神经化学研究。

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