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Biomedical subjects

N Hatotani

Publications and source records attributed to N Hatotani.

7 recordsLinked to original sources
PubMed1978

Stress-induced depression model in female rats--biochemical and histochemical investigation of brain monoamines.

Forced running stress induced a prolonged inactive state with the abolition of hormone-dependent cyclic behavior in some female rats which had already recovered from physical exhaustion. The state could be regarded as a "depression model" in these animals. In the biochemical study, norepinephrine in the hypothalamus was found to be significantly lowered in these animals. In the histochemical study, an increase of fluroescence intensity in nerve cell groups of the ascending norepinephrine system and a decrease of fluorescence intensity in nerve cells and terminals of the tubero-infundibular dopamine system were found in these animals. These findings were also seen in the rats which were examined immediately after the stress, but not in the rats which recovered their spontaneous and cyclic running activity in several weeks after the stress. These results suggest that changes of monoamine metabolism in the brain which is induced by the stress remains unrestored for a long time in the "depression model rats".

Animals↗
PubMed1977

Function of hypothalamo-pituitary thyroid axis in depressed patients.

Nineteen out of 51 depressed patients showed abnormal TSH response to TRH in terms of exaggerated, diminished and delayed responses. The basal value of T3 and its response to TRH were significantly lower in patients with delayed or diminished response than in the normal subjects. These results indicate that the dysfunction of the hypothalamo-pituitary thyroid axis plays an important role in the pathogenesis of depression.

Adult↗
PubMed1975

The effect of electrical stimulation of the hypothalamus and other brain areas on urea cycle enzymatic activities in the liver in rabbits--experimental studies on brain and liver interrelationship--.

Changes in urea cycle enzymatic activities in the liver induced by intracerebral electrical stimulation in rabbits with chronically implanted electrodes in the hypothalamus, the thalamus, and the limbic area were studied in comparison with these activities in non-stimulated controls. In stimulating the ventromedial nucleus of the hypothalamus, the two-hour sessions were followed by significantly reduced activity in arginase and the arginine synthetase system in the liver, but the six-hour stimulation sessions were followed by normal range activity in these enzymes. In stimulating the lateral hypothalamic area, the two-hour sessions were followed by only slightly reduced activity in the arginine synthetase system in the liver. Stimulation of the center median nucleus of the thalamus, the medial area of the amygdala and the dorsal hippocampus produced no significant changes in urea cycle enzymatic activities in the liver. The possibility that ammonia metabolism in the liver may be modified through some functional linkage between the brain and the liver was suggested.

Amygdala↗
PubMed1975

Studies on thyroid therapy and thyroid function in depressive patients.

A number of cases of depressed patients have latent hypothyroidism, possibly due to hypothalamo-pituitary dysfunction, and become refractory to antidepressant drugs. The dramatic effect or thyroid medication combined with tricyclic antidepressants is often observed in such persistently depressed patients. This effect seems to pertain to the catecholamine hypothesis of depression, but this requires further elucidation.

Adult↗