Drugs online research references
Am J Chin Med. 1998;26(2):127-32.
Effects of ginkgo biloba extract on impairment of learning induced by cerebral ischemia in mice.
Tadano T, Nakagawasai O, Tan-no K, Morikawa Y, Takahashi N, Kisara K.
Department of Pharmacology, Tohoku College of Pharmacy, Sendai, Japan.
The effect of Ginkgo biloba extract (GbE) on cerebral ischemia induced by 10-min bilateral occlusion of the carotid arteries in mice was studied. Severe impairment of memory was apparent when the passive avoidance test was carried out 48 hr after bilaterally induced ischemia. When GbE at doses of 50 and 100 mg/kg was given p.o. 1 hr before the 10-min occlusion, there was a significant improvement in memory. The i.p. injection of ifenprodil (30 mg/kg) also showed improvement on learning tasks. The p.o. administration of flavonoid, a fraction isolated from GbE, showed high step-through latency on scopolamine-induced amnesia. All these findings indicate that GbE is beneficial for clinical use in amnesia accompanied with cerebral vascular disease.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9799964&dopt=Abstract
Behav Brain Res. 1998 Oct;95(2):219-26.
Intra-amygdala infusions of scopolamine impair performance on a conditioned place preference task but not a spatial radial maze task.
McIntyre CK, Ragozzino ME, Gold PE.
Department of Psychology, University of Virginia, Charlottesville 22903, USA.
Lesions of the amygdala impair performance on a conditioned place preference (CPP) but not a spatial radial maze task. The role of cholinergic receptors within the amygdala in performance of these tasks was evaluated using intra-amygdala injections of the muscarinic receptor antagonist, scopolamine. Food deprived rats were trained on a CPP task, which consisted of four training trials on two arms of a radial eight-arm maze. One arm was consistently paired with a large amount of food (14 g) while the other arm was never baited. Prior to the fourth trial, rats received bilateral intra-amygdala infusions of the muscarinic receptor antagonist, scopolamine (SCOP; 5 microg/0.5 microl) or vehicle. On a retention test 24 h later, unoperated and vehicle-infused rats, but not SCOP-treated rats, spent significantly more time in the paired arm than chance (50%). Therefore, the scopolamine treatment appeared to block learning and/or memory on trial 4. The same rats were then trained on a radial maze task on the same apparatus, in which rats had access to all eight arms but only four were baited with food (1 pellet). Rats were trained until they reached criterion and then infusions were given prior to testing. SCOP treatment did not affect performance on the radial maze task. Thus, intact cholinergic mechanisms in the amygdala are necessary for learning or memory on a CPP task with a high reward component but not performance on a spatial radial maze task with a lower reward component.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9806441&dopt=Abstract
J Neural Transm. 1980;49(3):137-50.
Pharmacological analysis of a cholinergic receptor mediated regulation of brain norepinephrine neurons.
Engberg G, Svensson TH.
The significance of the cholinergic receptors within the noradrenergic nucleus locus coeruleus (LC) was analyzed by using single unit recording techniques and microiontophoretic drug application of various cholinergic and anticholinergic drugs. Physostigmine (25--50 micrograms/kg), intravenously administered, caused increased firing of LC neurons and this effect was blocked by scopolamine but not by methylscopolamine. Also nicotine (10--50 micrograms/kg i.v.) caused activation of LC neurons, an effect which was antagonized by the presumed nicotinic antagonist mecamylamine (8 mg/kg) as well as scopolamine (0.5 mg/kg i.v.). The cholinergic receptor within the LC showed specific muscarinic characteristics since microiontophoretic application of various muscarinic agonists caused excitation of LC units, whereas microiontophoretically applied nicotine had no effect. In addition, the acetylcholine (ACh)-induced excitation of the LC neurons was not blocked by nicotinic antagonists but was totally antagonized by the muscarinic agonist scopolamine. Scopolamine, when microiontophoretically applied onto the LC neurons, antagonized the stimulatory effect of systemically injected physostigmine but not that of nicotine. These results suggest that the stimulation of noradrenaline (NA) neurons in the LC by cholinergic drugs such as physostigmine is mediated via cholinergic, muscarinic receptors within this nucleus. The LC activation by nicotine is, however, an indirect effect, probably involving central ACh release and mediated via a non-cholinergic LC input.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7452224&dopt=Abstract
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