Subject(s)
Amine Oxidase (Copper-Containing) , Blood Proteins/antagonists & inhibitors , Brain/metabolism , Memory/physiology , Oxidoreductases Acting on CH-NH Group Donors/antagonists & inhibitors , Animals , Avoidance Learning/physiology , Benzylamine Oxidase/blood , Blood Proteins/immunology , Brain/enzymology , Brain/immunology , Brain/ultrastructure , Cattle , Dopamine/metabolism , Freund's Adjuvant/immunology , Male , Mitochondria/enzymology , Mitochondria/metabolism , Monoamine Oxidase/blood , Norepinephrine/metabolism , Oxidoreductases Acting on CH-NH Group Donors/blood , Oxidoreductases Acting on CH-NH Group Donors/immunology , Rats , Serotonin/metabolism , VaccinationABSTRACT
Effects of "delta-sleep inducing peptide" administration (60 micrograms/kg) to rats on the background of amphetamine action (2.5 mg/kg during 3 weeks) were studied. Activities of the enzymes of neurotransmitter turnover as well as the contents of biogenic amines in structures of motor cortex and caudate nucleus were investigated. Normalizing action of the peptide on the studied indices was found. It reflected the correction of the increased activity of dopaminergic and serotoninergic systems elevated as a result of amphetamine action. The suggestion was made that reconstruction of the interactions of neurotransmitter systems in brain providing adaptive behavior in animals was the main mechanism of delta-sleep inducing peptide's action.
Subject(s)
Amphetamine/pharmacology , Delta Sleep-Inducing Peptide/pharmacology , Dopamine Uptake Inhibitors/pharmacology , Animals , Biogenic Amines/metabolism , Caudate Nucleus/drug effects , Caudate Nucleus/metabolism , Drug Interactions , Male , Mitochondria/drug effects , Mitochondria/metabolism , Motor Cortex/drug effects , Motor Cortex/metabolism , Neurotransmitter Agents/metabolism , Rats , Rats, Wistar , Time FactorsABSTRACT
Single administration of the regulating peptide tuftsin Thr- Lys-Pro-Arg (300 micrograms/kg) was shown to affect the state of the transmitter systems in the brain of rats treated with the sedative drug haloperidol in a total dosage of 15 mg/kg within 30 days. Haloperidol therapy caused reciprocal alterations in the activity of monoamine oxidases A and B, in the levels of dopamine, noradrenaline, serotonin, and 5-hydroxyindolyl acetic acid, as well as a decrease in the rate of depolarization-dependent Ca(2+)-capture in the synaptosomes of the rat brain cortex and neostriatum (N. caudatus); under these conditions tuftsin normalized the parameters studied to a certain extent, which was more pronounced in N. caudatus. The peptide appeared to activate synaptic transfer in the dopaminergic nerve endings and to contribute to balance restoration in the neurotransmitter systems (particularly in the neostriatum) impaired by abnormalities.
