Drugs online research references
Brain Res. 1999 Jan 30;817(1-2):132-44.
Combined therapy affects outcomes differentially after mild traumatic brain injury and secondary forebrain ischemia in rats.
Jenkins LW, Lu Y, Johnston WE, Lyeth BG, Prough DS.
Department of Neurosurgery, University of Pittsburgh, 200 Lothrop Street, Suite B-400, Pittsburgh, PA 15260, USA.
Muscarinic and NMDA receptors contribute to post-traumatic hypersensitivity to secondary ischemia. However, the effect of these receptor antagonists on behavior and CA1 neuronal death after traumatic brain injury (TBI) with acute (1 h after TBI) forebrain ischemia has not been systematically assessed. We examined cognitive and motor dysfunction and the relationship of behavior deficits to neuronal death in this model using muscarinic and NMDA antagonists. Three behavioral groups (n=10&z.urule;group) of Wistar rats were subjected to mild TBI and 6 min of forebrain ischemia imposed 1 h after TBI with 45 days survival. Motor and spatial memory performance were assessed using the rotarod task and Morris water maze. Seven additional groups (n=6&z.urule;group) were evaluated only for CA1 death after 7 days survival following sham, individual or combined injury with and without drug treatments. Rats were given 0.3 mg/kg MK-801 (M) and 1.0 mg/kg scopolamine (S) alone or combined (M-S) before or 45 min after TBI. Rotarod performance was tested at days 1-5 and maze performance on days 11-15 and 40-44 after M-S treatment. The 7-day studies showed M-S treatment (p<0.01) reduced CA1 neuronal death better than either S or M alone. Behavioral groups had inadvertent post-ischemic hypothermia that decreased CA1 death and likely influenced behavioral morbidity. M-S given before TBI (p<0.01) decreased memory deficits on day 15, while M-S treatment given after TBI was ineffective. Unexpectedly, M-S treatment before or after TBI produced transient motor deficits (p<0. 01). Memory improvement occurred independent of CA1 death. Copyright 1999 Elsevier Science B.V.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9889350&dopt=Abstract
Zhongguo Yao Li Xue Bao. 1995 Jan;16(1):21-5.
Effects of isovanihuperzine A on cholinesterase and scopolamine-induced memory impairment.
Xiong ZQ, Tang XC, Lin JL, Zhu DY.
Department of Pharmacology, Shanghai Institute of Materia Medica, Chinese Academy of Sciences.
AIM: To study the effects of isovanihuperzine A (IVHA) on cholinesterase and scopolamine-induced memory deficit. METHODS: AChE and BuChE activities were determined by the colorimetric method of Ellman. The Ki value was determined by the plotting method of Lineweaver and Burk. In a behavioral test, rats were trained to perform a radial arm maze task using a partially baited procedure. RESULTS: The anti-AChE activity of IVHA was comparable to huperzine A (Hup-A), and was more potent than those of physostigmine and galanthamine with an IC50 value of 0.11 mumol.L-1. IVHA was a mixed competitive type with a Ki value of 32 nmol.L-1. It bound to AChE in a reversible manner. IVHA at a dose of 0.2 mg.kg-1 ip significantly reversed scopolamine-induced working memory and reference memory impairments in radial arm maze. CONCLUSION: IVHA is a new potential reversible AChE inhibitor and merits further study as a cognitive enhancer.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7771190&dopt=Abstract
liverpool.ac.uk
The interoceptive stimulus induced by clozapine (5 mg/kg, i.p.) has been characterized in an operant drug discrimination procedure in the rat using a wide range of receptor subtype-selective agonists and antagonists. Only the muscarinic receptor antagonist scopolamine generalized fully to clozapine (>80%). Partial generalization (defined here as 40% maximal generalization) was seen with the D1 receptor antagonist SCH 23390 (43% maximal generalization), the alpha1-adrenoceptor antagonist prazosin (67%) and the alpha2-adrenoceptor antagonist methoxyidazoxan (42%). All other specific agents tested induced <25% maximal generalization, including the alpha2-adrenoceptor antagonist yohimbine (24%), the histamine H1 receptor antagonist mepyramine (21%), the D2 antagonist typical neuroleptic haloperidol (23%), the D4 receptor antagonist L-745,870 (14%), the 5-hydroxytryptamine-1A (5-HT1A) receptor agonist S-14506 (8%), the 5-HT2A receptor antagonists ketanserin (0%) and M100907 (12%), the 5-HT2B/2C receptor antagonists SB 200646A (8%) and SDZ SER 082 (6%), and the 5-HT3 receptor antagonist ondansetron (0%). The clozapine discriminative stimulus was not blocked by the dopamine D1 receptor antagonist SCH 23390, or by the 5-HT1A receptor antagonist WAY 100635, when given concomitantly with clozapine. Although the results suggest that muscarinic antagonism plays a major role in the clozapine cue, the results have to be considered in the light of the full generalization to clozapine seen with various antipsychotic agents which have very low affinity for muscarinic receptors, including zotepine, quetiapine, JL13 and PNU 96415 (a finding replicated in rats from the same breeding colony as those which generalized to scopolamine). Thus, generalization to clozapine for antipsychotics with multiple affinities but with low muscarinic affinity is probably mediated by additive or perhaps supra-additive actions at other receptors, although extensive studies with various combinations of drug mixtures are required to validate this hypothesis.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9890260&dopt=Abstract
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