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Pharmacol Toxicol. 1987 Mar;60(3):206-9.
The effect of soman on potassium evoked 3H-acetylcholine release in the isolated rat bronchi.

Aas P, Malmei T, Fonnum F.

The in vitro exposure of rat bronchial smooth muscle to the acetylcholinesterase inhibitor soman (0-[1,1,2-trimethylpropyl]-methylphosphonofluoridate) reduced the potassium (51 mM) evoked release of 3H-acetylcholine (3H-ACh). Exposure to 1.0 and 100 microM soman for 15 min inhibited the acetylcholinesterase (AChE) activity completely and reduced the potassium evoked release by 23.1% and 34.4% respectively. In the presence of scopolamine (0.3 microM), however, there was a large enhancement (87.0%) of potassium evoked release during soman inhibited (100%) AChE-activity. Furthermore, soman (1.0 microM) did not reduce the spontaneous release of 3H-ACh. The results indicate that the presynaptic effect of soman is due to the enhanced concentration of ACh following AChE-activity inhibition in the synaptic region. This induces a stimulation of presynaptic muscarinic receptors and thereby modulation of the ACh release only during evoked release.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3588515&dopt=Abstract




J Pharmacol Exp Ther. 1994 Sep;270(3):881-92.
Possible involvement of the activation of voltage-sensitive calcium channels in the ameliorating effects of nefiracetam on scopolamine-induced impairment of performance in a passive avoidance task.

Yamada K, Nakayama S, Shiotani T, Hasegawa T, Nabeshima T.

Department of Neuropsychopharmacology and Hospital Pharmacy, Nagoya University School of Medicine, Japan.

We investigated the effects of various types of calcium channel antagonists on the amelioration by nefiracetam [N-(2,6-dimethylphenyl)-2-(2-oxo-1-pyrrolidinyl) acetamide, DM-9384] of scopolamine-induced impairment of performance in a passive avoidance task in mice. The reversal of the scopolamine-induced impairment of performance by nefiracetam showed a bell-shaped plot. Both i.p. and i.c.v. injection of L-type calcium channel antagonists such as nifedipine and flunarizine attenuated the ameliorating effects of nefiracetam, although diltiazem had no effect. Neomycin, an N-type calcium channel antagonist, also attenuated these effects of nefiracetam in a dose-dependent manner. Further, LaCl3 but not NiCl2 showed inhibitory effects on the amelioration by nefiracetam. These results suggest that the activation of high-voltage-activated, but not low-voltage-activated, calcium channels is involved in the ameliorating effects of nefiracetam on scopolamine-induced impairment of performance in a passive avoidance task.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7932200&dopt=Abstract




Neuropharmacology. 1993 Jun;32(6):535-42.
UCB 29120, a novel, potential psychotropic agent, alters norepinephrine and dopamine content of rat brain.

Elrod K, Raikoff K, Wulfert E, Hanin I.

Department of Pharmacology and Experimental Therapeutics, Loyola University Chicago Stritch School of Medicine, Maywood, Illinois.

UCB 29120 belongs to a novel family of compounds possessing interesting behavioral and physiological properties. Behavioral studies in the rat have revealed the ability of the compound to inhibit scopolamine-induced amnesia while physiological studies demonstrated a significant drug-induced hypothermic response and increase corticosterone plasma levels following acute administration of the compound. In the present study we examined the time-course effects of acute administration of UCB 29120 on levels of catecholamines (norepinephrine, NE; dopamine, DA), indoleamines (serotonin, 5-HT) and metabolites (3,4-dihydroxyphenylacetic acid, DOPAC; 5-hydroxyindoleacetic acid, 5-HIAA) in the rat hypothalamus. Hippocampal, septal and striatal tissue content of the same were also examined at the longest time point employed. In the hypothalamus, UCB 29120 induced significant decreases in NE content 30 min following administration which persisted for at least an additional 30 min, while significant increases in DA and/or DOPAC (and the DOPAC/DA ratio) were measured as early as 5 min following administration and persisted through at least a total of 120 min. Similar, significant changes in dopaminergic parameters were also evident in the other three brain regions at 120 min post-administration. No significant alterations in hypothalamic 5-HT or 5-HIAA were measured at any time point. Acute administration of UCB 29120 may selectively influence catecholaminergic neurotransmitter systems in rat brain.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8336818&dopt=Abstract













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