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Biomedical subjects

N B Thoa

Publications and source records attributed to N B Thoa.

At least 55 records · Page 3Linked to original sources
PubMed1972

6-Hydroxydopa depletion of brain norepinephrine and the function of aggressive behavior.

A significant increase in shock-induced aggression occurs in the rat 4 days after an intraventricular injection of 90 micrograms of 6-hydroxydopa. Both fluorescent histology and biochemical assay demonstrate that brain norepinephrine is reduced by 90 micrograms of 6-hydroxydopa, while brain dopamine remains unaltered. This suggests that one form of aggressive behavior (shock-induced aggression) is modulated through a central noradrenergic system.

Aggression↗
PubMed1972

Rat fighting behavior: serum dopamine- -hydroxylase and hypothalamic tyrosine hydroxylase.

Male Sprague-Dawley rats were subjected to 4 weeks of daily periods of immobilization stress. One of two experimental groups was allowed 1 month of recovery. After 4 weeks of stress, there was a significant increase in shockinduced fighting, in the activity of serum dopamine-beta-hydroxylase, and in the activity of hypothalamic tyrosine hydroxylase. The concentration of hypothalamic norepinephrine was not decreased. After 4 weeks of recovery, only serum dopamine-betahydroxylase activity returned to normal; it therefore appears that longterm stress may increase central catecholamine synthesis. possibly resulting in a persistent increase in aggressive behavior.

Aggression↗
PubMed1972

Inhibition of release of dopamine- -hydroxylase and norepinephrine from sympathetic nerves by colchicine, vinblastine, or cytochalasin-B (hypogastric nerve stimulation-exocytosis-microtubules-microfilaments-guinea pig).

Stimulation of the hypogastric nerve to the guinea pig vas deferens in the presence of phenoxybenzamine produced an enhanced release of both dopamine-beta-hydroxylase (EC 1.14.2.1) and norepinephrine. Addition of colchicine, vinblastine, or cytochalasin-B to the incubation medium caused an almost complete inhibition of release of both the amine and the enzyme. Colchicine and cytochalasin-B produced a blocking effect but did not, however, modify the ratio of dopamine-beta-hydroxylase to norepinephrine recovered in the bath fluid. The findings indicate that norepinephrine and dopamine-beta-hydroxylase are released from sympathetic nerve terminals by exocytosis and that this process is dependent upon the integrity of both microtubules and microfilaments.

Animals↗
PubMed1971

Proportional release of norepinephrine and dopamine- -hydroxylase from sympathetic nerves.

Dopamine-beta-hydroxylase(DBH), the enzyme that catalyzes the conversion of dopamine to norepinephrine, is localized in the vesicles containing catecholamine in sympathetic nerves. This enzyme is released with norepinephrine when the nerves to the guinea pig vas deferens are stimulated in vitro, and the amount of enzyme discharged increases as the length of stimulation periods increases. The amount of DBH released is proportional to the amount of norepinephrine released, and the ratio of norepinephrine to DBH discharged into the incubation medium is similar to that in the soluble portion of the contents of the synaptic vesicles from the vas deferens. These data are compatible with the release of the neurotransmitter norepinephrine and DBH from symnpathetic nerves by a process of exocytosis.

Animals↗
PubMed1971

Enhanced release of dopamine- -hydroxylase from sympathetic nerves by calcium and phenoxybenzamine and its reversal by prostaglandins.

Dopamine-beta-hydroxylase (EC 1.14.2.1), an enzyme localized in sympathetic synaptic vesicles, was released together with norepinephrine during in vitro stimulation of the hypogastric nerve that innervates the vas deferens of the guinea pig. Stimulation of the nerve in the presence of high concentrations of calcium (7.5 mM) or phenoxybenzamine caused a marked increase in the amounts of the enzyme and norepinephrine released into the bath. The augmentation of release of dopamine-beta-hydroxylase by 7.5 mM calcium or phenoxybenzamine was reversed by prostaglandin E(2). These findings suggest that the release of the sympathetic neurotransmitter, norepinephrine, occurs by a process of exocytosis in which the vesicular content of soluble dopamine-beta-hydroxylase is also released. The depolarization-induced exocytosis, which is stimulated by calcium, may be affected by prostaglandin E(2) or phenoxybenzamine through inhibition or enhancement of the actions of calcium in the release process.

Animals↗