Subject(s)
Acetylcholinesterase/drug effects , Cholinesterase Reactivators/pharmacology , Acetylcholinesterase/metabolism , Animals , Cholinesterase Reactivators/therapeutic use , Drug Interactions , Ganglionic Blockers/pharmacology , Humans , Organophosphate Poisoning , Parasympatholytics/pharmacology , Phosphorylation/drug effects , Poisoning/drug therapy , Poisoning/enzymology , Structure-Activity RelationshipABSTRACT
Having estimated the rat behaviour in the open-field test, M-cholinolytics were divided into different groups. Haloperidol normalised the disturbance in the behaviour induced by one group M-cholinolytics and had no effect with the other group. The former group seems to have an explicit dopaminergic activity. The groups seem to correspond to different mechanisms of the behavioural activity.
Subject(s)
Behavior, Animal/drug effects , Parasympatholytics/pharmacology , Receptors, Muscarinic/drug effects , Animals , Behavior, Animal/physiology , Dose-Response Relationship, Drug , Exploratory Behavior/drug effects , Exploratory Behavior/physiology , Male , Rats , Receptors, Muscarinic/physiology , Reflex/drug effects , Reflex/physiologyABSTRACT
Antioxidants and disulphide bond reducing agents have shown the central N-cholinolytic effect and prevented nicotinic-induced contraction of isolated smooth muscle preparation (ISMP). N-cholinolytic pediphen and antioxidant ionol reduced disulphide bond in the supernatant of mouse brain, but sulphydryl-oxidant agents 5'5-Dithiobis (2-nitrobenzoic acid) abolished N-cholinolytic effect of pediphen on ISMP. It is concluded that reduction of disulphide bond of N-cholinoceptor is a molecular mechanism of its blockade.
Subject(s)
Butylated Hydroxytoluene/pharmacology , Neurons/drug effects , Nicotine , Receptors, Cholinergic/drug effects , Sympatholytics/pharmacology , Animals , Brain/drug effects , Brain/metabolism , Disulfides/metabolism , In Vitro Techniques , Mice , Muscle Contraction , Muscle, Smooth/drug effects , Nicotine/antagonists & inhibitors , Rats , Receptors, Cholinergic/metabolism , SpectrophotometrySubject(s)
Behavior, Animal/physiology , Conditioning, Classical/physiology , Animals , Avoidance Learning/drug effects , Avoidance Learning/physiology , Behavior, Animal/drug effects , Conditioning, Classical/drug effects , Female , Orientation/drug effects , Orientation/physiology , Parasympatholytics/pharmacology , Rats , Time FactorsSubject(s)
Orientation/physiology , Animals , Escape Reaction/physiology , Exploratory Behavior/physiology , Female , Male , Mathematics , Rats , Rest/physiologyABSTRACT
It was found therapeutic-preventive effectiveness of antioxidants (1,4-dihydropyridine derivatives) at poisoning with malathion insecticide. The effect of 1,4-dihydropyridine derivatives can be attributed to a prevention of lipid peroxidation. Antioxidants do not affect the toxicity of 0,0-dimethyl-0-2,2-dichlorvinylphosphate. Thus, antioxidants are pathogenetic drugs for treatment of poisonings with cholinesterase inhibitors.
Subject(s)
Antioxidants/pharmacology , Cholinesterase Inhibitors/poisoning , Animals , Antioxidants/therapeutic use , Dihydropyridines/pharmacology , Dihydropyridines/therapeutic use , Lipid Peroxidation/drug effects , Malathion/poisoning , Male , Mice , RatsABSTRACT
The effect of central M- and N-cholinolytics on Fe++-ascorbate-dependent lipid peroxidation (LP) in the rat brain homogenate was studied in vitro. Central N-cholinolytics were shown to inhibit LP. Pediphen was the most active drug. Central M-cholinolytics were not active. Pediphen and an antioxidant ionol equally decreased LP in the rat brain after carbon tetrachloride intoxication (3 ml/kg). Ionol and pediphen had N- and not M-cholinolytic effect. It is suggested that membrane stabilization by N-cholinolytics is dependent on the antioxidant effect of the drugs. These data show an important role of LP in the function of cholinergic system.
