Leonard T O, Lydic R
Department of Anesthesia, Pennsylvania State University, College of Medicine, Hershey 17033, USA.
Neuroreport. 1995 Jul 31;6(11):1525-9. doi: 10.1097/00001756-199507310-00015.
This study tested the hypothesis that inhibition of nitric oxide synthase (NOS) in the medial pontine reticular formation (mPRF) would cause decreased acetylcholine (ACh) release. Microdialysis of cat mPRF permitted measurement of ACh during states of wakefulness, non-rapid eye movement (NREM) sleep and rapid eye movement (REM) sleep. ACh release during microdialysis with Ringers (control) was compared to ACh release during microdialysis with 10 mM NG-nitro-L-arginine (NLA). The NOS inhibitor NLA caused a significant reduction in ACh released from the mPRF during wakefulness, NREM sleep, and REM sleep. This reduction in mPRF ACh release elicited by NLA suggests that nitric oxide (NO) contributes to cholinergic neurotransmission in the pontine reticular formation.
抑制脑桥内侧网状结构（mPRF）中的一氧化氮合酶（NOS）会导致乙酰胆碱（ACh）释放减少。对猫的mPRF进行微透析，可在清醒、非快速眼动（NREM）睡眠和快速眼动（REM）睡眠状态下测量ACh。将用林格氏液（对照）进行微透析期间的ACh释放与用10 mM NG-硝基-L-精氨酸（NLA）进行微透析期间的ACh释放进行比较。NOS抑制剂NLA导致在清醒、NREM睡眠和REM睡眠期间从mPRF释放的ACh显著减少。NLA引起的mPRF中ACh释放减少表明一氧化氮（NO）有助于脑桥网状结构中的胆碱能神经传递。
