Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: DrugBank:EXPT02427 (Atropine)
 3,300 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Previous work has shown that N-methyl-D-aspartate (NMDA) receptor activation inhibits muscarinic receptor-mediated phosphoinositide hydrolysis in brain slices. To further explore the potential interactions between NMDA receptors and cholinergic receptors, the effects of cholinergic agonists and NMDA on [3H]norepinephrine (NE) release from rat cortical slices were determined. Slices were labeled with [3H]NE, washed and treated with various agonists by transferring the slices through a series of vials at 1-min intervals. Radioactivity remaining in the medium was then quantitated to determine the fractional release of [3H]NE from the slices. Carbachol (30-3000 microM) slightly stimulated [3H]NE release from a basal level of 0.10 to approximately 0.35 fractional release by itself and significantly enhanced the effect of 250 microM NMDA (3.6 fractional release for NMDA and 5.3 for carbachol + NMDA) in a concentration-dependent manner. Carbachol (1 mM) increased the maximal response but had no effect on the EC50 of NMDA. Atropine (1 microM) significantly attenuated the effect of carbachol alone and the potentiation of NMDA-evoked [3H]NE release by carbachol, whereas d-tubocurarine (10 microM) inhibited the effect of carbachol alone but had no effect on the enhancement of the NMDA response by carbachol. Mecamylamine (100 microM) inhibited the effect of carbachol alone, but also inhibited the NMDA-evoked response with an IC50 of 16 microM. The nicotinic agonist, dimethylphenylpiperazinium (DMPP) stimulated [3H]NE release (approximately 0.4 fractional release at 30 microM) and also potentiated NMDA-stimulated [3H]NE release (2.0 above NMDA alone). d-Tubocurarine, but not atropine, partially inhibited DMPP-stimulated [3H]NE release, but neither antagonist altered the enhancement of NMDA-stimulated [3H]NE release by DMPP.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cholinergic modulation of N-methyl-D-aspartate-evoked [3H]norepinephrine release from rat cortical slices. 842 31

The pharmacology of auditory brain-stem evoked potentials (ABEP) pathways is poorly understood. There are anecdotal reports on the involvement of various neurotransmitters but they were not investigated systematically. The aim of this study was to investigate the effects on ABEP of muscarinic and nicotinic blockers, administered into the cerebral ventricles. Atropine sulfate, d-Tubocurarine and saline were injected stereotactically into the lateral cerebral ventricle of anesthetized male rats. Auditory clicks were given at a rate of 20 s(-1). ABEP recording was performed before and 30 min after injection. Pre- and post-injection peak latencies and peak-to-peak amplitudes of positive waves were compared for each animal. Atropine reduced the amplitudes of waves P1, P3 and P4 and increased mildly the brain stem transmission time. d-Tubocurarine reduced the amplitudes of P1 and P4 with no significant effect on the peak latencies. Saline injection had no effect on any of the parameters. These results show that both cholinergic systems are involved in ABEP generation or transmission. Mechanism of action could be either direct inhibition of afferent pathways or indirect effect, via modulating efferent pathways.
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PMID:Effects of cholinergic blockers on auditory brain-stem evoked potentials in rats. 1040 22


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