ABSTRACT
The experiments on rats have shown that the effect of millimeter range electromagnetic radiation on the bioelectric brain activity is dependent on the initial functional state of central nervous system. Microwaves are able to cause a nonspecific electroencephalographic reaction of synchronization and probably the lower the bioelectric brain process dynamics of active rats. Enrichment of electrocorticograms with high-frequency rhythms and increase in degree of bioelectric brain dynamics can be observed in narcosis conditions. The appearance of biological resonance in the brain of narcotized rats preliminary injected aminazin by pulse-modulated microwaves is noted. This is expressed as epileptiform convulsive activity in electrocorticogram. It has been shown that the nonlinear dynamics method may provide a reliable characterization of changing bioelectric brain activity under of nonionized electromagnetic fields. It is possible to modulate the bioelectric brain activity by microwaves to change the functional state of central nervous system and probably of the whole organism.
Subject(s)
Brain/radiation effects , Electromagnetic Fields , Microwaves , Alpha Rhythm , Anesthesia , Animals , Beta Rhythm , Brain/drug effects , Brain/physiology , Chlorpromazine/pharmacology , Cortical Synchronization , Dopamine Antagonists/pharmacology , Electroencephalography , Radiation, Nonionizing , Rats , Seizures/etiology , Time FactorsABSTRACT
The experiments in rats and rabbits revealed a correlation among the body temperature, the peripheral temperature threshold, central (thermosensitive neurons) thermoregulatory responses, and the temperature of phasic transition of brain lipids three latter parameters rising during experimental fever. The composition of phospholipids changed in hypothalamic tissues, i.e. the level of saturated fatty acids radicals increased.
Subject(s)
Body Temperature Regulation , Brain/metabolism , Lipid Metabolism , Animals , Brain/physiology , Female , Hot Temperature , Hypothalamus/physiology , Male , Neurons, Afferent/physiology , Rabbits , RatsABSTRACT
The experiments on rats and rabbits have shown that exogenous phosphatidyl choline (PC) was capable of altering the body temperature and bioelectrical activity of posterior hypothalamus neurons following intravenous and intracerebroventricular administration. Intracerebroventricular PC was more effective in raising the body temperature of rats. The experiments on rabbits have demonstrated that the influence of PC (intravenous administration) on the body temperature depended on the initial body temperature. In rabbits, the changes in the impulse activity of certain non-thermosensitive posterior hypothalamus neurons induced by intracerebroventricular PC administration were found to be dependent on the initial firing rates. PC inhibited the increase in bioelectrical activity of thermosensitive neurons in posterior hypothalamus caused by the rise in the brain temperature secondary to body temperature elevation.
Subject(s)
Body Temperature/drug effects , Hypothalamus, Posterior/drug effects , Hypothalamus/drug effects , Neurons/drug effects , Phosphatidylcholines/pharmacology , Animals , Carbachol/pharmacology , Hypothalamus, Posterior/physiology , Liposomes/administration & dosage , Neurons/physiology , Norepinephrine/pharmacology , Rabbits , RatsABSTRACT
Experiments on rats were made to study the effect on the body temperature of the rat of intracerebroventricular injection of venoms of Indian cobra, North American rattle snake, and Central Asian shchitomordnik. It was established that the rise of rectal temperature by 1.5-2.0 degrees C after 90 min was evoked by cobra venom alone. That increase in the body temperature was not prevented by pretreatment with the protein synthesis inhibitors anisomycin or cycloheximide, but was completely abolished by intraperitoneal injection of sodium salicylate. The reduction of hyperthermia was also attained with intracerebroventricular injection of the prostaglandin synthetase inhibitor valtoren as well as with subsequent (following snake venom) injections of arecoline or calcium ions.
Subject(s)
Body Temperature/drug effects , Snake Venoms/toxicity , Animals , Body Temperature Regulation/drug effects , Crotalid Venoms/toxicity , Drug Interactions , Elapid Venoms/toxicity , Female , Fever/chemically induced , Injections, Intraventricular , Rats , Time Factors , Viper Venoms/toxicityABSTRACT
It has been demonstrated in rat experiments that the central action of PGE2 results in body temperature rise associated with a reduction in the functional activity of hypothalamic adrenergic systems. In contrast to PGE2 and the beta-adrenomimetic isoproterenol, the alpha-adrenomimetics noradrenaline, mezaton and clonidine were shown to lower body temperature. In the rabbit, clonidine and PGE2 were found to have opposing effects on the neuronal activity of the anterior hypothalamus.
Subject(s)
Brain/drug effects , Fever/chemically induced , Prostaglandins E/pharmacology , Receptors, Adrenergic, alpha/drug effects , Animals , Body Temperature Regulation/drug effects , Dinoprostone , Fever/metabolism , Hypothalamus/drug effects , Hypothalamus/metabolism , Injections, Intraventricular , Neurons/drug effects , Norepinephrine/metabolism , Rabbits , RatsABSTRACT
It has been found in experiments on unanesthetized rabbits that arecoline administered to the lateral ventricle of the brain produced an action which was opposite to that of leukocytic pyrogen. It inhibited the activity of individual neurons of the posterior hypothalamus and decreased the body temperature, with this decrease being attended by the signs of intensified heat emission. Arecoline injection coupled with the central action of PGE2 was followed by an increase in the neuronal activity in the posterior hypothalamus and reduction of hyperthermal response.
Subject(s)
Body Temperature Regulation , Fever/physiopathology , Hypothalamus, Posterior/physiopathology , Hypothalamus/physiopathology , Interleukin-1 , Neurons/physiology , Action Potentials/drug effects , Animals , Body Temperature/drug effects , Dinoprostone , Hyperthermia, Induced , Prostaglandins E/pharmacology , Proteins/pharmacology , RabbitsABSTRACT
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.
Subject(s)
Body Temperature/drug effects , Prostaglandins E/antagonists & inhibitors , Animals , Benactyzine/analogs & derivatives , Benactyzine/pharmacology , Clonidine/pharmacology , Diphenylacetic Acids/analogs & derivatives , Diphenylacetic Acids/pharmacology , Hemicholinium 3/pharmacology , Isoproterenol/analogs & derivatives , Isoproterenol/pharmacology , Methysergide/pharmacology , Nicotine/pharmacology , Norepinephrine/pharmacology , Oxotremorine/pharmacology , Phenoxybenzamine/pharmacology , Propranolol/pharmacology , Rats , Serotonin/pharmacologyABSTRACT
It was shown in experiments on unanesthetized rats with prostaglandin E2 (PGE2) hyperthermia, not preventable by aspirin that intraventricular (into the lateral ventricle) injections of arecoline, noradrenaline, 5-hydroxytryptamine (5-HT), histamine, and calcium ions and intraperitoneal eserine injection were capable of decreasing body temperature. PGE2 hyperthermia was not prevented by aspirin, but it was reduced by eserine. After the administration of arecoline and nicotine into the third ventricle of unanesthetized rabbits with PGE2 hyperthermia body temperature decreased as well. The effect of arecoline and 5-HT was reproducible in the same animals. The data are suggestive of the existence in the heat loss centre of mechanisms including cholinergic neurons whose activity was not completely suppressed by PGE2.