Abstract
Regulation of acetylcholine metabolism varied in brain slices from hippocampus and septum which have different proportions of cholinergic nerve cell bodies and nerve endings. Anoxia (0% oxygen) inhibited acetylcholine synthesis (-77%) and its calcium-dependent release (-87%) from hippocampal slices but had no effect on synthesis or release by septal slices. [1,5-14C]Citrate incorporation into acetylcholine was higher in septum than in hippocampus, which suggested that citrate metabolism differs regionally. (-)Hydroxycitrate, a specific inhibitor of ATP citrate (pro3S)-lyase (EC 4.1.3.8), reduced [U-14C]glucose incorporation into acetylcholine more in septal than in hippocampal slices. 14CO2 production from glucose or citrate was similar in control and experimental conditions in the two regions. These findings indicate that acetylcholine metabolism varies regionally, which may partially explain the selective vulnerability of certain brain areas to anoxia and other metabolic insults.
Highlights
Anoxia (0%oxygen) inhibited acetylcholine synthesis (-77%) and its calcium-dependent release (-87%) fromhippocampal slices buthad no effect on synthesis or release by septal slices. [1,5-14C]Citrate incorporationinto acetylcholine was higher in septumthan in hippocampus, which suggested that citrate metabolismdiffers regionally. (-)Hydroxycitrate, a specific inhibitor of ATP citrate-lyase (EC 4.1.3.8), reduced [U-'4C]glucose incorporationinto acetylcholinemore in septal than in hippocampalslices. 14C02production fromglucose or citrate was similar in control andexperimentalconditionsin the two regions
These findings indicate that acetylcholine metabolism varies regionally, which may partially explain the selective vulnerability of certain brain areas to anoxia and other metabolic insults
Acetylcholine and oxidative metabolism were examined in brain slices from the septum which contains a high proportion of cholinergic nerve cell bodies and the hippocampus with primarilycholinergic nerve terminals (Kimura et al, 1981)
Summary
Gibson, 1981; Peterson and Gibson, 1982) without alterations in theconcentration of acetylcholine. Male Wistar rats (200-300 g) were from Charles Rivers Breeding physiologically important, rapidly turning over compartment in the brain (Blass and Gibson, 1978), or that low oxygen inhibits the release of acetylcholine which subsequently impairs synthesis (Gibson andPeterson, 1982; Petersonand Gibson, 1982). Acetylcholine Metabolism and "C02 Production-Rats (200-300 g) were decapitated, and the whole brain was removed and placed in ice-cold buffer (pH 7.4): 5.0 mM KC1, 2.3 mMCaC12, 1.3 mM MgS04, 141mM NaCI, and 10.0mM Na2HP04
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