Drugs online research references
crl.hpk.co.jp
The effects of somatosensory stimulation on the regional cerebral blood flow (rCBF) response were studied in unanesthetized monkeys under modulations of the glutamatergic and cholinergic systems using [15O]H2O and positron emission tomography (PET). Under a saline condition, vibrotactile stimulation elicited a significant increase in the rCBF response in the contralateral somatosensory cortex. The systemic administration of scopolamine, a muscarinic cholinergic receptor antagonist, resulted in the dose-dependent reduction of the rCBF response to the stimulation. The rCBF response abolished by scopolamine was recovered by the administration of physostigmine, a cholinesterase inhibitor in a dose-dependent manner. In addition, D-cycloserine, a partial agonist at the glycine site coupled to N-methyl-D-aspartate (NMDA) receptors, also restored the scopolamine-abolished rCBF response. The regional cerebral metabolic rate of glucose (rCMRglc) response, measured with [18F]-2-fluoro-2-deoxy-D-glucose, was not affected by the administration of scopolamine, physostigmine and/or D-cycloserine. The systemic administration of (+)-3-amino-1-hydroxy-2-pyrrolidone (HA-966), an antagonist of the glycine modulatory site on the NMDA receptors, induced the dose-dependent suppression of the rCBF response to the stimulation. The rCBF response abolished by HA-966 was restored by D-cycloserine, but not by physostigmine. The rCMRglc response was partially but significantly reduced by the administration of HA-966, and its reduction was restored by D-cycloserine, but not by physostigmine. These findings provided pharmacological evidence for an interaction between cholinergic and glutamatergic neuronal systems, the latter of which mediates the former by downstream regulation, in the functional rCBF response to somatosensory stimulation.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9689457&dopt=Abstract
Am J Physiol. 1998 Jun;274(6 Pt 1):G997-1004.
Lithocholyltaurine interacts with cholinergic receptors on dispersed chief cells from guinea pig stomach.
Raufman JP, Zimniak P, Bartoszko-Malik A.
Department of Internal Medicine, University of Arkansas for Medical Sciences, Little Rock, Arkansas 72205-7199, USA.
Although bile acids damage gastric mucosa, the mechanisms underlying tissue injury induced by these agents are not well understood. To determine whether bile acids alter gastric secretory function, we investigated the actions of sodium cholate, deoxycholate, lithocholate, and their taurine and glycine conjugates on a highly homogeneous population of gastric chief cells. Lithocholyltaurine (LCT), a particularly injurious bile acid, caused a threefold increase in pepsinogen secretion (detectable with 100 nM and maximal with 10 microM LCT). When combined with other secretagogues, increasing concentrations of LCT caused progressive inhibition of carbamylcholine (carbachol)-induced pepsinogen secretion but did not alter CCK- or 8-bromo-cAMP-induced secretion. Taurine and unconjugated lithocholate did not alter basal or carbachol-induced secretion. These observations suggested that LCT is a partial cholinergic agonist. To test this hypothesis, we examined the actions of the cholinergic antagonist atropine on LCT-induced pepsinogen secretion. Atropine (10 microM) abolished carbachol- and LCT-induced pepsinogen secretion. Likewise, carbachol (0.1 mM) and LCT (1 mM) induced an atropine-sensitive, two- to threefold increase in cellular levels of inositol 1,4,5-trisphosphate. We examined the actions of LCT on binding of the cholinergic radioligand [N-methyl-3H]scopolamine ([3H]NMS) to chief cells. Half-maximal inhibition of [3H]NMS binding was observed with approximately 0.5 mM carbachol and 1 mM LCT. These results indicate that the bile acid LCT is a partial agonist for muscarinic cholinergic receptors on gastric chief cells.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9696723&dopt=Abstract
Biol Pharm Bull. 1998 Jul;21(7):698-703.
Effects of N-[2-(1-azabicyclo[3,3,0]octan-5-yl)ethyl]2-nitroaniline fumarate (SK-946), a novel cognition activator, on learning and memory in rodent models.
Suzuki T, Hirooka K, Kanda K, Hirooka H, Furusawa K.
Pharmaceutical Laboratory, Sanwa Kagaku Kenkyusho Co., Ltd., Mie, Japan.
We examined the effects of N-[2-(1-azabicyclo[3,3,0]octan-5-yl)ethyl]2-nitroaniline fumarate (SK-946) on cognition in various rodent models. SK-946 slightly suppressed spontaneous motor activity, but had no effect on scopolamine-induced motor facilitation. SK-946 ameliorated scopolamine-, pirenzepine-, cycloheximide- and electric shock-induced passive avoidance deficits in rodents when administered before acquiring the training. In an active avoidance test, SK-946 accelerated avoidance acquisition in the later half of training without a marked increase in lever-pressing. In more reliable models of cognitive disorders, i.e. an AF64A intracerebroventricular infusion model using the step-through passive avoidance test, an aged rat model using the step-down passive avoidance test and methylazoxymethanol (MAM)-induced microencephalic rat model using the Morris water maze test, SK-946 ameliorated impaired learning and memory. These results suggest an ability of SK-946 to enhance cognitive functions.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9703252&dopt=Abstract
Herbs and Pharmaceuticals Online ||
Hair Million herbal formula for hair loss and hair growth ||
Wellstreet online pharmacy for click-order prescription medications ||
Altace Online Pharmacy ||
Rx Drugs USA, Prescription Drugs Online Pharmacy ||
Insurance plans and information ||
Insurance policies for all purposes ||
Antibiotics and prescription medications online literature ||