NMDA受体
氯胺酮
乙酰胆碱
苯环己定
地唑西平
药理学
美金刚
谷氨酸受体
化学
胆碱能的
神经递质
微透析
麻醉
内分泌学
内科学
神经科学
医学
中枢神经系统
心理学
受体
作者
Ralph Lydic,Helen A. Baghdoyan
出处
期刊:Sleep
[Oxford University Press]
日期:2002-09-01
卷期号:25 (6): 615-620
被引量:68
标识
DOI:10.1093/sleep/25.6.615
摘要
Ketamine induces a dissociated state of consciousness by binding to the phencyclidine binding site within the ion channel gated by the N-methyl-D-aspartate (NMDA) receptor. The brain regions and neurotransmitter systems mediating ketamine-induced alterations in arousal remain incompletely understood. This study used in vivo micro-dialysis to test the hypothesis that ketamine alters acetylcholine (ACh) release in the medial pontine reticular formation (mPRF). Acetylcholine (ACh) release, sleep, and breathing were quantified following systemic ketamine administration. Microdialysis was used to deliver the NMDA-channel blocker dizocilpine maleate (MK-801) and the R(−)-isomer of ketamine into the mPRF while measuring ACh release. N/A N/A N/A Systemically administered ketamine disrupted normal sleep-cycle organization, reduced mPRF ACh release, and significantly slowed rate of breathing. Dialysis delivery of MK-801 to the mPRF significantly decreased respiratory rate and mPRF ACh release. Dialysis delivery to the mPRF of the R(−)-ketamine isomer significantly decreased mPRF ACh release. Decreased mPRF ACh release caused by systemically administered ketamine was mimicked by mPRF dialysis delivery of MK-801 and the R(−)-ketamine isomer. These data are consistent with the conclusion that systemically administered ketamine may alter arousal and breathing, in part, by altering cholinergic neurotransmission in the mPRF.
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