首页> 外文期刊>Neuroscience Letters: An International Multidisciplinary Journal Devoted to the Rapid Publication of Basic Research in the Brain Sciences >Activation of CB1 cannabinoid receptors in rat hippocampal slices inhibits potassium-evoked cholecystokinin release, a possible mechanism contributing to the spatial memory defects produced by cannabinoids.
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Activation of CB1 cannabinoid receptors in rat hippocampal slices inhibits potassium-evoked cholecystokinin release, a possible mechanism contributing to the spatial memory defects produced by cannabinoids.

机译:大鼠海马切片中CB1大麻素受体的激活抑制了钾诱发的胆囊收缩素的释放,这可能是造成大麻素产生的空间记忆缺陷的机制。

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摘要

Cannabinoid use is known to disrupt learning and memory in a number of species. cholecystokinin (CCK) release and CCK receptors have been implicated in spatial memory processes in rodents. Rat hippocampal CCK interneurons express cannabinoid 1 receptors (CB1). The CB1 agonist R(+)WIN 55,212-2 (WIN+), at 1 and 10 micromol, strongly inhibited potassium-evoked CCK release from rat hippocampal slices, while the inactive isomer S(-)WIN,55,212-3 (WIN-) had no effect. CCK release from cerebral cortical slices was not altered by WIN+.
机译:已知使用大麻会破坏许多物种的学习和记忆。胆囊收缩素(CCK)释放和CCK受体与啮齿动物的空间记忆过程有关。大鼠海马CCK内部神经元表达大麻素1受体(CB1)。 CB1激动剂R(+)WIN 55,212-2(WIN +)的浓度为1和10微摩尔,强烈抑制大鼠海马切片中钾诱发的CCK释放,而无活性异构体S(-)WIN,55,212-3(WIN-)没有效果。 WIN +不会改变大脑皮层切片的CCK释放。

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