[Role of the catecholaminergic system of the brain in addiction to alcohol (review)].
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Biomedical subjects
Publications and source records attributed to M M Borisov.
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Following the injection of guanethidine (25 mg/kg) to rats from the first day of life during 2 weeks, over 70% of sympathic neurons in the stellate ganglion die. If the injections are carried out during 4 weeks, over 99% of neurons die. The injection of guanethidine to mice during 5 weeks did not result in the destruction of nerve elements in the ganglion, as compared with the control.
The amount of cells in stellate ganglia of rat was decreased by chemical sympathectomy to 30% of the normal amount. At the age of two months sympathectomized rats have no pressor reflexes to asphyxia and femoral nerve stimulation. These responses are restored at the age of four months. The electron-microscopic and fluorescence-microscopic data show that the growth of axons in the remaining adrenergic neurons of sympathectomized animals takes place at the age between two and four months.
Prolonged administration of guanethidine (20 mg/kg) to newborn rats caused a marked reduction in the number of cells in stellate ganglia. The administration of guanethidine for 14 days decreased the amount of cells to 30% of the normal (partial sympathectomy), and for 28 days--to 0.5% (complete sympathectomy). At the age of two months the blood pressure pressor reflexes to asphyxia and femoral nerve stimulation were absent in both groups of the sympathectomized animals. These responses, however, were restored in the partially sympathectomized animals at the age of four months. No restoration took place in the completely sympathectomized animals. The electron microscopic studies of neurons in the partially sympathectomized animals showed the presence of a great number of neurofibrils. According to literature data this fact was typical of cells in which an active growth of axon fibers took place.
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It was shown that 3,12-b-dimethyl-octahydroindol-(2,3-a) quinolyzine (at the dose of 1/6 of LD50) exerted an antialcohol effect in mice and rats which is probably due to an increased content of the brain 5-hydroxytryptamine resulting from selective inhibition of its deamination.
The effect of immunization of rats with the conjugated antigen morphine-bovine serum albumin synthetized by the authors on the analgetic activity of morphine hydrochloride has been investigated. Morphine binding antibodies were shown to appear in the blood of rats during immunization. The spleen demonstrated mononuclear cells also capable of morphine binding. It has been established that immunization of rats with the above synthetic antigen makes them tolerate the pharmacological effects of the narcotic. Morphine at a dose of 5 mg/kg is not capable of inducing an inherent increase in the threshold of pain sensitivity in immunized rats. Immunization also slightly diminishes the morphine effect at a dose of 20 mg/kg on the EEC. Prolonged daily administration of morphine does not remove morphine tolerance due to immunization.
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