[Sources of scientific information on the problem of environmental protection].
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Biomedical subjects
Publications and source records attributed to A L Bandman.
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Stereotypy and locomotor hyperactivity caused by subcutaneous injection of apomorphine (1-5 mg) were quantitated with an "Animex-DSE" motility meter. Intraperitoneal administration of galantamin in a dose of 2.5 mg/kg 10 minutes before apomorphine reversed the latter's effect. However, when injected in a similar way 40 minutes before, it exerted no action on behavioral effects of apomorphine. Intraperitoneal administration of amizyl in a dose of 1 mg/kg completely prevented antagonism of galantamin to apomorphine activity but did not potentiate its effect on the locomotor activity in the animals. The data obtained show that the effect of the cholinergic system on dopaminergic mediation in individual brain structures may be modulating in nature. The experimental data are discussed in the light of the present-day concepts of the function of dopamine receptors in the striatum and mesolimbic systems of the brain.
Motional excitement (ME), dopamine (DA) and homovanillic acid (HVA) content in the caudate nucleus of rats who were injected with morphine in doses of 2 and 10 mg/kg intraperitoneally after amyzil (40 mg/kg) given via the same route were studied to clarify the character of the action of narcotic analgetics on animals' behavior and DAN metabolism under conditions of imbalance between the cholinergic and dopaminergic neuromediator systems of the striatum, induced by central cholinolytics. Amyzil injection was shown to lower HVA level with no changes in DA content (the mediator turnover rate seems to decrease) and to start ME. Under these conditions morphine, in the presence of the induced imbalance of the mediator systems, exhibits a correcting action, elevating HVA level and apparently speeding DA turnover. The biochemical shifts described are accompanied by ME abolition. Possible mechanisms of the action of narcotic analgetics on dopaminergic mediation in the striatum are discussed.
Naphthylvinylpyridine (NVP) in the cat cerebral cortex (50 mg/kg) and in the mouse brain (100 and 250 mg kg) caused inhibition of choline acetyltransferase (ChA) and didn't influence the acetyl- and butyrilcholinesterase activity and acetylcholine (Ach) content in the mouse brain. NVP (25 mg/kg) failed to influence the ChA activity. Pretreatment with NVP (25 and 250 mg/kg) increased the duration of hexenal sleep in mice greatly, and a dose of 250 mg/kg (but not of 25 mg/kg) enhanced the atropine activity in mice poisoned with armine. NVP (250 mg/kg) reduced the release of Ach from the cerebral cortex of a cat, spontaneous and evoked by atropine and electrical stimulation of the reticular formation of the brain stem. A conclusion was drawn that the pharmacological effect of NVP when the latter was applied in combination with atropine and armine could be connected with the anti-Cha action and the inhibition of the newly-formed Ach, rather than with depression of the microsomal enzymes.
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