PubMed · 11094053
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B A Kingwell, G L Jennings, A M Dart. 2000-11-28. Exercise and endothelial function.. https://doi.org/10.1161/01.cir.102.22.e179
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Recently, the potent cholinesterase inhibitor (-)-huperzine A (HupA) was demonstrated to protect neuronal and glial cells against the cytotoxicity of beta-amyloid (Abeta). Since the unnatural (+)-HupA is a much less potent inhibitor, it was of interest to examine the stereoselectivity of cellular protection by the two isomers. In the present study, effects of (+)- and (-)-HupA on Abeta(25-35)-induced injury were compared in PC12 and NG108-15 neuroblastoma cell lines. Following a 24 h exposure to 1 microM Abeta(25-35), cell survival was markedly reduced, but preincubation with (+)-HupA or (-)-HupA (0.1-10 microM) enhanced survival significantly. The potency of (-)-HupA and (+)-HupA in protecting against Abeta toxicity was similar. This result contrasted with the stereoselectivity of cholinesterase inhibition in vitro and in vivo, in which (-)-HupA is about 50-fold more potent than (+)-HupA. It is concluded that the neuroprotective properties of HupA enantiomers have no relation to anti-cholinesterase activity.
The local anesthetic lidocaine suppresses different pain conditions when administered systemically. Part of the antinociceptive effect appears to be mediated via receptor mechanisms. We have previously shown that muscarinic and nicotinic agonists that produce antinociception increase the intraspinal release of acetylcholine. In the present study it was hypothesized that systemically administered lidocaine is acting through the same mechanisms as cholinergic agonists and affects the intraspinal release of acetylcholine. Microdialysis probes were placed in anesthetized rats for sampling of acetylcholine. Ten and 30 mg/kg lidocaine injected intravenously significantly increased the intraspinal release of acetylcholine. The effect of lidocaine could be reduced by pretreatment with intraspinally administered atropine or mecamylamine. Our results suggest that the antinociceptive effect produced by systemically administered lidocaine is mediated through an action on muscarinic and nicotinic receptors.
The distribution of the high-affinity choline transporter (CHT) was determined in the human and macaque monkey spinal cord using in situ hybridization histochemistry and immunohistochemistry. Signals for CHT mRNA were observed in somatic motor neurons, sympathetic preganglionic neurons, and neurons in the medial part of lamina VII. The mRNA for CHT was co-localized in single neurons with the mRNAs for vesicular acetylcholine transporter and cholineacetyltransferase. These same cholinergic neuronal groups were labeled by immunohistochemistry for human CHT. Of somatic motor neurons, smaller cell bodies of gamma-motor neurons were labeled very intensely, whereas larger cell bodies of alpha-motor neurons showed various degrees of labeling from weak to moderately intense. Human CHT is thus a novel cholinergic marker, which not only labels cholinergic neurons, but also reveals their heterogeneity.