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At least 667 records · Page 37Linked to original sources
PubMed1981

[Effect of synaptically active substances on the hyperthermic effect of prostaglandin E2 in rats].

It was established in experiments on unanesthetized rats given intraventricular injections of drugs that hyperthermic effect of prostaglandin E2 (PGE2) was markedly weakened by administering clofelin while isoproterenol had no appreciable effect on PGE2 effects were not prevented by noradrenaline, 5-hydroxytryptamine, phenoxybenzamine, propranolol, deseril, nicotine, metamyzyl and IEM-506. Preliminary administration of oxotremorine and hemicholinium-3 averted PGE2 effect. The disorders of the thermo-regulation centers caused by excess PGE2 are likely to be counterbalanced by the central effect of some synaptically active drugs which affect in particular the function of cholinergic synapses and alpha-adrenoreceptors.

Animals↗
PubMed1981

[Effect of psychotropic drugs on cerebral Ca-activated ATPase in vitro].

Neuroleptics, particularly haloperidol and perphenazine, inhibit the activity of brain Ca, Mg-ATPase to a greater extent than the antidepressants benactizin and amphetamine. The actomyosin-like Ca-ATPase is far less sensitive to the psychotropic drugs than Ca,Mg-AtPase. It is suggested that the inhibition of brain Ca,Mg-AtPase by neuroleptics may play a certain role in their antipsychotic action.

Amphetamine↗
PubMed1981

[Role of M- and N-cholinergic biosystems of the brain in the mechanisms responsible for optokinetic, postoptokinetic, and reversed postoptokinetic nystagmus].

In rabbits, the effects of different inhibitors: of Achesterase--nivalin, of M-cholinergic receptors--metamizyl and N-cholinergic receptor--eterophen on the optokinetic nystagmus (OKN), positive optokinetic afternystagmus (OKAN) and reversed postoptokinetic nystagmus (RPN) revealed that in mechanism of the OKH, OKAN and RPN both colinergic systems took part: N-cholinergic system in the OKH and OKAN and M-cholinergic system in RPN formation.

Acetylcholine↗
PubMedDate not supplied

[Neurochemical mechanisms of the effect of ACTH on aggressive-defensive behavior in rats].

It was found that ACTH increased fear and aggressive-defensive behavior in pairs of male rats in response to electrical stimulation. The parameters were the threshold values of squeak reactions, risings and fights, the frequency of fights and the duration of standing in a posture of threat. The ACTH influence was similar to the M-cholinomimetic effect. It increased against the background of M-cholinoreceptors' excitation but did not change in essential under the action of H-cholinoreceptors. An assumption has been made of the extraadrenal action of ACTH on affective aggression. The mechanism of the effect involves facilitation of excitation of the central M-cholinoreceptors.

Adrenocorticotropic Hormone↗
PubMedDate not supplied

[Neuropharmacological analysis of electroacupuncture analgesia].

It was established in experiments on conscious rats using concurrent recording of pain sensitivity and evoked potentials that the leading part in electroacupuncture analgesia is played by endogenous opioid peptides. However, numerous pharmacological substances can alter the level of electroacupuncture analgesis suggesting the participation in its genesis of different mediator cerebral systems. In the animals resistant to acupuncture, administration of morphine did not produce marked analgetic effect.

5-Hydroxytryptophan↗
PubMed1983

[Effect of N- and M- cholinoblockaders on experimental epileptogenesis].

It has been shown in chronic experiments on rabbits with epileptogenic foci provoked by microinjections of penicillin into the dorsal hippocamp that the N-cholinoblockers gangleron (3 mg/k, intravenously) and etherophen (5-10mg/kg, intravenously) possess marked anticonvulsant activity. Diphenin (50 mg/kg, intraperitoneally) was less potent. The M-cholinoblocker methamizil (1 mg/kg, intravenously), on the contrary, potentiated the epileptiform seizures. Emphasis is laid on the necessity of the goal-oriented synthesis and search for agents that would exhibit a "purely" central N-cholinoblocking action with a purpose of applying such agents as antiepileptic drugs. It is not recommended using the M-cholinoblockers for such purposes.

Animals↗
PubMed1980

[Effect of amizil and arecoline on the interaction of Na+ and Ca2+ ons in the cerebral nerve endings of rats].

A study was made of the effect of the central cholinolytic benactizin and cholinomimetic arecoline on the uptake of 45Ca and 22N by rat brain synaptosomes. It was shown that benactizin in a dose of 40 mg/kg increased the incorporation and uptake of 45Ca and decreased the incorporation and uptake 22Na. Arecoline (2.5 mg/kg) increased the accumulation of 22Na and decreased the content of 45Ca in the synaptosomes. It is assumed that benactizin activates Ca-channels and inactivates Na-K-channels and inhibits or produces no action on Ca-channels.

Animals↗
PubMed1978

[Experience in treating vascular parkinsonism with metamysil].

The paper is concerned with a study of the effect of metamizil in 45 patients with different forms of vascular parkinsonism. It was established that metamizil exerts a positive effect on the development of neurological symptoms (rigidity, bradykinesia, tremor) in mild and moderately expressed degrees of lesions. In most of the cases the drugs appeared effective in doses of 0.001 g thrice daily, and in separate cases 0.001 g 6 times daily. In the majority of patients metazil was tolerated without significant side effects. In some patients the side effects (vertigo, dryness in the mouth) were slightly expressed. The effect of treatment was seen after 2 days up to 2 weeks and lasted during the whole course of treatment and sometimes after it. Metamizil possessing a moderate sedative action, as well as spasmolytical and hypotensive is indicated for patients with vascular parkinsonism.

Aged↗