Drugs online research references
Neurol Res. 1994 Jun;16(3):194-200.
Quantitative assessment of quinolinic acid-induced striatal toxicity in rats using radioligand binding assays.
Levivier M, Holemans S, Togasaki DM, Maloteaux JM, Brotchi J, Przedborski S.
Department of Neurosurgery, Universite Libre de Bruxelles-Erasme Hospital, Belgium.
To validate specific, sensitive and quantitative markers of the rat model of Huntington's disease produced by the intrastriatal injection of quinolinic acid, we used striatal homogenate binding assays for [3H]MK-801-labelled N-methyl-D-aspartate receptors, [3H]SCH 23390-labelled D1 and [3H]sulpiride-labelled D2 dopamine receptors, [3H]CGS 21680-labelled adenosine A2 receptors, [3H]GBR 12935-labelled dopamine uptake sites, [3H]hemicholinium-3-labelled high affinity choline uptake sites and [3H]PK 11195-labelled glial cells, in 3 groups of rats: 1) lesioned only, 2) pretreated with MK-801, an antagonist of the N-methyl-D-aspartate receptor, to assess the non-N-methyl-D-aspartate-mediated toxicity of quinolinic acid, and 3) pretreated with MK-801 plus scopolamine, an anticholinergic drug that prevents MK-801 neuronal toxicity. [3H]MK-801 and [3H]PK 11195 are sensitive markers of quinolinic acid toxicity. In addition, [3H]SCH 23390, [3H]CGS 21680 and [3H]hemicholinium-3, are found to be specific markers of quinolinic acid-induced toxicity on striatonigral and striatopallidal projecting neurons, and on large interneurons, respectively. MK-801 pretreatment prevented the quinolinic acid-induced reduction in binding of [3H]MK-801, [3H]SCH 23390 and [3H]CGS 21680 but failed to do so for [3H]sulpride and [3H]hemicholinium-3, suggesting that quinolinic acid may act by mechanisms other than direct activation of N-methyl-D-aspartate receptors. Combined pretreatment with MK-801 and scopolamine increased the protection against quinolinic acid, suggesting an involvement of the cholinergic system.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7936089&dopt=Abstract
Pharmacol Biochem Behav. 1976 May;4(5):561-8.
Modulation of the aversive qualities of shock through a central inhibitory cholinergic system in the rat.
Houser VP.
Evidence has been supplied which suggests that a central inhibitory cholingeric (i.e., muscarinic) system may be involved in modulating the aversive qualities of electric shock in the rat. Central cholinergic stimulation via the administration of pilocarpine or arecoline the threshold for grid shock, while central acting anticholinergics (i.e., scopolamine and atropine) produced decrements in the threshold. Peripheral acting anticholinergics (e.g., methyl scopolamine, methyl atropine) were less potent than central acting drugs given in equivalent doses, while peripheral cholinergic stimulants (i.e., neostigmine, carbachol) were inactive. In addition, only the central acting stimulant pilocarpine, and not carbachol, was able to block the decrements noted in response to scopolamine hydrobromide administration. Finally, only arecoline, and not nicotine, was able to elevate the aversive threshold indicating that muscarinic receptor sites are probably involved in mediating the effects of central cholinergic stimulants.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=951435&dopt=Abstract
Jpn J Pharmacol. 1993 May;62(1):81-6.
Protective effect of R(-)-1-(benzo[b]thiophen-5-yl)- 2-[2-(N,N-diethylamino)ethoxy]ethanol hydrochloride (T-588), a novel cerebral activator, against experimental cerebral anoxia.
Ono S, Kitamura K, Maekawa M, Hirata K, Ano M, Ukai W, Yamafuji T, Narita H.
Research Laboratories, Toyama Chemical Co., Ltd., Japan.
Effects of R(-)-1-(benzo[b]thiophen-5-yl)-2-[2- (N,N-diethylamino)ethoxy]ethanol hydrochloride (T-588) on normobaric hypoxia, histotoxic anoxia by KCN and complete ischemia by decapitation were investigated in mice. T-588 (30-100 mg/kg, p.o.) showed a significant and dose-dependent prolongation of the survival time in all of the models studied. Bifemelane (100-300 mg/kg, p.o.) was also protective against all the models. Tacrine was protective against hypoxia but had no effect on anoxia and ischemia. Imipramine was protective against anoxia, but shortened the survival time of hypoxic mice. It had no effect on ischemia. The anti-hypoxic effect of T-588 was completely inhibited by pretreatment with scopolamine (1 mg/kg, i.p.), while the anti-anoxic effect was partially inhibited. Its effect on the ischemia was not affected by scopolamine. Hypoxia decreased the cerebral contents of ATP, phosphocreatine and glucose and increased the contents of lactate in mice. T-588 had no effect on these changes. Bifemelane prolonged pentobarbital-induced sleeping time in mice with the doses inducing anti-anoxic action, but T-588 did not. These results suggest that the activation of the CNS cholinergic system is involved as one of the mechanisms for the anti-anoxic action of T-588.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8101887&dopt=Abstract
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