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J Neural Transm. 1998;105(10-12):1171-85.
Glucose minimally attenuates scopolamine-but not morphine-induced deficits on a water maze alternation task.

Means LW, Edmonds SM.

Department of Psychology, East Carolina University, Greenville, NC 27837, USA.

In a previous study, daily injections of glucose, 100 and 250 mg/kg i.p., in Sprague-Dawley rats failed to either facilitate acquisition or to ameliorate scopolamine- or morphine-induced deficits on a water maze alternation task (Means, et al., 1996). The present study demonstrates that daily injections of 1 g/kg minimally ameliorates a scopolamine-induced deficit on the water maze alternation task in Sprague-Dawley rats. However, daily glucose injections of 1, 2 and 4 g/kg failed to improve performance during acquisition or to diminish morphine-induced deficits on the task. The failure of daily administration of glucose to facilitate acquisition or reverse morphine-induced deficits was not due to the daily injection procedure nor to stress elevated glucose levels resulting from exposure to the task. It is suggested that the effects of glucose on memory are task dependent, with facilitation being more easily demonstrated on tasks for which animals have an innate bias to perform the correct response or the ability to acquire in very few trials.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9928886&dopt=Abstract




J Biol Chem. 1994 Dec 23;269(51):32522-7.
Sequestration of muscarinic acetylcholine receptor m2 subtypes. Facilitation by G protein-coupled receptor kinase (GRK2) and attenuation by a dominant-negative mutant of GRK2.

Tsuga H, Kameyama K, Haga T, Kurose H, Nagao T.

Department of Biochemistry, Faculty of Medicine, University of Tokyo, Japan.

Sequestration of m2 receptors (muscarinic acetylcholine receptor m2 subtypes), which was assessed as loss of N-[3H]methylscopolamine ([3H]NMS) binding activity from the cell surface, was examined in COS 7 and BHK-21 cells that had been transfected with expression vectors encoding the m2 receptor and, independently, vectors encoding a G protein-coupled receptor kinase (GRK2) (beta-adrenergic receptor kinase 1) or a GRK2 dominant-negative mutant (DN-GRK2). The sequestration of m2 receptors became apparent when the cells were treated with 10(-5) M or higher concentrations of carbamylcholine. In this case, approximately 40% or 20-25% of the [3H]NMS binding sites on COS 7 or BHK-21 cells, respectively, were sequestered with a half-life of 15-25 min. In cells in which GRK2 was also expressed, the sequestration became apparent in the presence of 10(-7) M carbamylcholine. Approximately 40% of the [3H]NMS binding sites on both COS 7 and BHK-21 cells were sequestered in the presence of 10(-6) M or higher concentrations of carbamylcholine. When DN-GRK2 was expressed in COS 7 cells, the proportion of [3H]NMS binding sites sequestered in the presence of 10(-5) M or higher concentrations of carbamylcholine was reduced to 20-30%. These results indicate that the phosphorylation of m2 receptors by GRK2 facilitates their sequestration. These results are in contrast with the absence of a correlation between sequestration and the phosphorylation of beta-adrenergic receptors by the GRK2 and suggests that the consequences of phosphorylation by GRK2 are different for different receptors.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7798253&dopt=Abstract




J Neural Transm. 1998;105(10-12):1193-7.
Changes in apparent in vivo binding of [3H]raclopride and [3H]N-methylspiperone induced by oxotremorine.

Kobayashi K, Gee A, Hosoi R, Inoue O.

School of Allied Health Sciences, Osaka University Faculty of Medicine, Suita, Japan.

The effects of muscarinic agonist, oxotremorine (0.3 mg/kg), and antagonist, scopolamine (0.5 mg/kg), on in vivo [3H]raclopride (RAC) and [3H]N-methylspiperone (NMSP) binding were investigated. Following tracer administration to control or pretreated mice, binding potentials, and the rate constants k3 and k4 were determined by kinetic analysis. Oxotremorine resulted in a 70% increase in striatal RAC binding potential compared with controls. RAC and NMSP showed almost identical decreases in k3 (40%), whereas k4 for RAC was unexpectedly decreased by 64%. Scopolamine resulted in no significant changes in RAC or NMSP binding. These results, in combination with previous data obtained in reserpinized mice, show that 1) competition by endogenous ligand may not be the only factor influencing the magnitude of apparent in vivo receptor binding, and 2) interneuronal communication may be partly mediated by changes in the rates of ligand-receptor binding.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9928888&dopt=Abstract













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