ABSTRACT
No significant change occurs in the total cerebral level of norepinephrine, dopamine, and histamine in rats of 1--36 months age, whereas the serotonin (5-HT) level is increasing. During the maturation period the hypothalamic levels of catecholamines and histamine are increasing. Between 2--36 months of life the hypothalamic norepinephrine level decreases while 5-HT, 5-HIAA, and histamine do not change. Role of the age-related changes of brain biogenic amines in disturbances of neuroendocrine feedback mechanisms is discussed.
Subject(s)
Biogenic Amines/analysis , Brain Chemistry , Age Factors , Aging , Animals , Brain Chemistry/drug effects , Brain Stem/analysis , Dopamine/analysis , Histamine/analysis , Hydroxyindoleacetic Acid/analysis , Levodopa/pharmacology , Male , Norepinephrine/analysis , Rats , Serotonin/analysis , Sexual MaturationABSTRACT
Thirty minutes after the administration of DMBA (5 mg i. v.) to rats the level of norepinephrine, dopamine, serotonine (5-HT) and 5-IIIAA in the hypothalamus was decreased, while monoamines levels in the brain stem and hemispheres was unchanged. After benz(a) anthracene (5 mg i.v.) treatment the level of 5-HT in rat hypothalamus was decreased, but catecholamines and 5-HIAA levels were not changed. Pretreatment with L-DOPA abolished the elevation of the threshold of hypothalamic sensitivity to estrogen suppression, induced by 20-methylcholanthrene in rats, and alpha-methyl-DOPA enhanced. It is suggested that the central (hypothalamic) mechanisms participate in the release of the carcinogenic effect of polycylic hydrocarbons in rats.
Subject(s)
9,10-Dimethyl-1,2-benzanthracene/pharmacology , Benz(a)Anthracenes/pharmacology , Biogenic Amines/metabolism , Brain/drug effects , Animals , Brain/metabolism , Castration , Diethylstilbestrol/pharmacology , Dihydroxyphenylalanine/analogs & derivatives , Dihydroxyphenylalanine/pharmacology , Drug Tolerance , Female , Hypothalamus/drug effects , Hypothalamus/metabolism , Levodopa/pharmacology , Male , Methylcholanthrene/pharmacology , Rats , Time FactorsABSTRACT
Three hours after the dimethylhydrazine-3H (DMH) treatment specific radioactivity in the male rat pituitary, adrenal cortex, and the testes was higher than in the liver by 53, 85, and 108%, respectively. Tritium incorporation into the hypothalamus was higher than that by the liver, cerebral cortex, and the brain stem by 33, 69, and 44%, respectively. Three hours after the diethyl-hydrazine-3H (DEH) treatment the specific activities of the pituitary and the testes in male rats were higher than that of the liver by 57 and 108%, respectively. A single DMH and DEH administration to male rats in a dose of 21 mg per kg body weight resulted in a significant decrease of the pituitary FSH level (by 63 and 53%, respectively). The data obtained were indicative of a marked influence of the carcinogenic dialkylhydrazines on the rat neuroendocrin system.
Subject(s)
Follicle Stimulating Hormone/metabolism , Hydrazines/metabolism , Pituitary Gland, Anterior/drug effects , Pituitary Gland/drug effects , Animals , Depression, Chemical , Dimethylhydrazines/metabolism , Dimethylhydrazines/pharmacology , Female , Hydrazines/pharmacology , Hypothalamus/metabolism , Male , Organ Specificity , Pituitary Gland, Anterior/metabolism , Rats , Sex FactorsABSTRACT
The hypothalamic levels of noradrenaline (NA), dophamine (DA), serotonine (5-HT), 5-hydroxyindolacetic acid (5-HIAA) were found to be decreased in male rats 24 hours after subcutaneous injection of 1,2-dimethylhydrazine (SDMH) in a dose of 21 mg/kg. During 3 to 12 hrs after the SDMH treatment the hypothalamic level of NA was decreased, whereas the 5-HT turnover became greater. The hypothalamic histamine level increased 30 min after the SDMH injection only. In the brain stem and the great hemispheres the biogenic amine level displayed no significant changes under the effect of SDMH. The endocrine-metabolic changes due to the selected SDMH effect on the hypothalamic biogenic amine level are supposed to be of great significance in the realization of the carcinogenic action of SDMH in rats.
