Nitric oxide synthase inhibition decreases pontine acetylcholine release.
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.
Leonard
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Department of Anesthesia, Pennsylvania State University, College of Medicine, Hershey 17033, USA.
Lydic
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D000818:Animals; D001120:Arginine / Q000031:analogs & derivatives* / Q000494:pharmacology; D002415:Cats; D004791:Enzyme Inhibitors / Q000494:pharmacology*; D008297:Male; D017551:Microdialysis; D019331:NG-Nitroarginine Methyl Ester; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors*; D011149:Pons / Q000187:drug effects* / Q000378:metabolism; D012890:Sleep / Q000187:drug effects; D012895:Sleep, REM / Q000187:drug effects
D004791:Enzyme Inhibitors; D001120:Arginine; D019001:Nitric Oxide Synthase; D019331:NG-Nitroarginine Methyl Ester