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Biomedical subjects

M B Youdim

Publications and source records attributed to M B Youdim.

348 records · Page 20Linked to original sources
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Iron deficiency induces reversal of dopamine dependent circadian cycles: differential response to d-amphetamine and TRH.

Rats made nutritionally iron-deficient (ID) have significantly diminished haemoglobin, serum iron and hypothermic response to d-amphetamine (15 mg/kg). The reduction of d-amphetamine induced hypothermia is comparatively greater in the dark than in the light period. Neither TRH (1 mg/kg) nor CG 3703, a peptidase resistant TRH analogue (1 mg/kg), induced hypothermia in control of ID animals. However, in combination with d-amphetamine, TRH and CG 3703 did not alter the hypothermic effect observed initially with d-amphetamine. In contrast to control animals, ID rats treated with saline or d-amphetamine (15 mg/kg) exhibited a greater degree of motor activity in the light as compared to the dark period. However, the overall activity (light plus dark) was unchanged in the ID group. The motor activity in response to TRH or CG 3703 was not changed as a result of iron-deficiency. These differential responses may be due to a more pronounced action of d-amphetamine on dopaminergic system, which is known to be changed in iron-deficiency, and of TRH and CG 3703 on the noradrenergic neurones.

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Minimal brain damage induced by early iron deficiency: modified dopaminergic neurotransmission.

The reports that iron-deficiency anemia in human subjects induces behavioral changes was investigated in rats made nutritionally iron-deficient. The most prominent features of these animals were: the unchanged metabolism of the neurotransmitters noradrenaline, dopamine and serotonin, profound reduction of brain nonheme iron, the selective diminution of dopamine D2 receptor number (measured by Bmax), modification of dopamine-dependent behaviors and reduction of learning processes. The induction of these changes and their recovery with iron supplementation are age- and time-dependent phenomena. In newborn rats, however, the consequences of iron deficiency are irreversible, even after long-term iron supplementation. The results point to the profound effect iron metabolism can have on the long-term development and function of dopaminergic neurotransmission. These findings may not be totally unexpected, since iron distribution in the brain is highly localized in dopaminergic-peptidergic regions, such as the globus pallidus, substantia nigra, red nucleus, thalamus, caudate nucleus and nucleus accumbens. In some regions its concentration is higher than that found in the liver, the site of iron metabolism.

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Regulation of central and peripheral carbohydrate reserves after selective inhibition of enzyme monoamine oxidase: comparison between fed and starved rats.

1. Maintenance of brain, liver and heart glycogen after selective inhibition of enzyme monoamine oxidase with clorgyline and deprinil was studied in normally fed or starved rats. 2. The administration of clorgyline to fed rats produces an important decrease in glycogen of the brain after 3 h of injection whereas the same treatment to starved rats resulted in complete exhaustion of brain glycogen stores. 3. Deprinil administration provoked a complete disappearance of glycogen in brain in fed rats after one and three hours of the injection but the same dose given to starved rats had a similar effect only after one hour since three hours after brain glycogen reserves of starved rats were close to the control values. 4. Clorgyline did not modify hepatic glycogen in fed rats but in starved rats in increase after three hours of administration took place. 5. Deprinil decreased liver glycogen in fed rats but the starved rats showed increases after one and three hours. 6. Heart glycogen increased in fed rats after clorgyline injection but starved rats showed slight decreases. Deprinil decreased cardiac glycogen slightly in fed as well as starved rats. 7. After one hour of deprinil injection glycemia was at the lowest value in fed rats but the decrease in starved rats was less marked. Three hours after deprinil or clorgyline administration both groups showed increases in glycemia. 8. Marked differences in the degree of MAO inhibition between fed and starved rats were observed after clorgyline and deprinil administration. The brain of starved rats showed only 49% inhibition whereas fed rats had 91% enzyme inhibition after three hours of deprinil treatment.

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