Drugs online research references
duke.edu
The authors report that the expression of a conditioned odor aversion is impaired in preweanling rats when they are conditioned on Postnatal Day 12 and tested under the influence of scopolamine hydrobromide (0.2 or 0.5 mg/kg, intraperitoneal) after a 48-hr, but not after a 2-hr, retention interval (Experiment 1). This effect of scopolamine is not dependent on maturation of the cholinergic system between Days 12 and 14 (Experiment 2), nor is it due to peripheral mechanisms (Experiment 3). When pups are reexposed to the unconditioned stimulus (footshock) before drug administration, performance on the 48-hr retention test is not impaired by scopolamine (Experiment 4). These findings demonstrate that the cholinergic system may be critical for the retrieval and expression of long-term or weak memories in young rats. However, the expression of active memories (recent or recently reactivated) may not be dependent on the cholinergic system to the same extent as is the expression of inactive memories.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9733197&dopt=Abstract
Brain Res. 1998 Sep 14;805(1-2):20-8.
The effect of hypothalamic peptide YY on hippocampal acetylcholine release in vivo: implications for limbic function in binge-eating behavior.
Hagan MM, Castaneda E, Sumaya IC, Fleming SM, Galloway J, Moss DE.
Department of Psychiatry, University of Cincinnati Medical Center, Box 670559, Cincinnati, OH 45267-0559, USA.
Central injection of peptide YY (PYY) in sated rats produces the most powerful stimulating effect of food intake known to date. The neural mechanisms by which PYY regulates appetite are not clear but may be important because abnormal levels of PYY have been implicated in the neurobiology of bulimia nervosa. Interactions between brain acetylcholine (ACh) and PYY had not been studied. Therefore, the present experiments were designed to explore the in vivo release of ACh from the hippocampus (HPC) of rats in response to hypothalamic infusion of PYY. Hippocampal ACh release was found to increase 400% in response to 10 microg PYY. In a separate experiment, blockade of the same area of the HPC with bilateral intracerebral injections of 3.5 microg scopolamine did not affect intake stimulated by intrahypothalamic injection of 4 microg PYY. Furthermore, a third experiment showed, for the first time, that PYY (2.5-10.0 microg) can elicit robust feeding when infused directly into the HPC. The significance of these findings to the activation of limbic functions such as memory, reinforcement, and obsessional processes that accompany human binge-eating syndromes is discussed. Copyright 1998 Elsevier Science B.V.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9733907&dopt=Abstract
Chem Pharm Bull (Tokyo). 1998 Aug;46(8):1265-73.
Synthesis and muscarinic activity of a series of quinolines and naphthalenes with a 1-azabicyclo[3.3.0]octane moiety.
Suzuki T, Usui T, Oka M, Suzuki T, Kataoka T.
Drug Discovery Research Laboratory, Sanwa Kagaku Kenkyusho Co., Ltd., Mie, Japan.
In order to discover a medicine effective against Alzheimer's disease, we synthesized a series of quinoline derivatives having a characteristic 1-azabicyclo[3.3.0]octane amine ring, and performed pharmacological evaluation of them. Acetylcholine esterase inhibitory activities of these derivatives were unexpectedly weak. Tests for central nervous muscarinic cholinergic receptor binding affinity indicated that these compounds had higher affinities to muscarinic M1 receptors than to M2 receptors. A series of naphthalene derivatives substituted with the 1-azabicyclo[3.3.0]octane ring were also synthesized and muscarinic M1 and M2 receptor binding affinity determined. These compounds had much higher affinity for M1 receptors than the quinoline derivatives, and 1-[N-(1-azabicyclo[3.3.0]octan-5-yl)methyl-N-methylamino]-4-nitronaph tha lene showed the highest affinity and selectivity. The ability of this compound to improve cognitive function was assessed using the passive avoidance test in scopolamine-induced mice.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9734314&dopt=Abstract
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