Monoamine Oxidase Activity In Rats Research Articles

The Effect of 3-Hydroxypyridine and Succinic Acid Derivatives on Hippocampal Monoamine Oxidase Activity in Rats with Alloxan-Induced Diabetes

The effect of the original, domestically manufactured, derivatives of 3-hydroxypyridine and succinic acid (emoxipine, reamberin and mexidol) on the dynamics of monoamine oxidase (MAO-A and MAO-B) activity was studied as compared with the hippocampal level of biogenic amines (serotonin and dopamine) during the first two weeks of alloxan-induced diabetes in rats. It was shown that during this period the hippocampus develops a buildup of dopamine and serotonin against the background of unchanged MAO-A and MAO-B activities. It was established that a 14-day administration of emoxipine, reamberin and mexidol in animals with alloxan-induced DM at doses equivalent to the human therapeutic range prevented an increase in paleocortical serotonin and dopamine levels. Succinate-containing drugs (reamberin and mexidol) induced a parallel decrease in the MAO-B activity in the Ammon’s horn of diabetic animals. Mexidol, which is a co-derivative of 3-hydroxypyridine and succinic acid, induced additionally decreased the hippocampal MAO-A activity. In terms of the severity of the above effects, reamberin and mexidol were not inferior to α-lipoic acid which was used as a reference drug. An isolated derivative of 3-hydroxypyridine (emoxipine), in contrast to reamberin, mexidol and α-lipoic acid, promoted normalization of paleocortical serotonin and dopamine levels but did not affect hippocampal MAO-A and MAO-B activities in rats with alloxan-induced DM. 3-hydroxypyridine derivatives (emoxipine and mexidol), in contrast to reamberin and α-lipoic acid, induced no transient increase in MAO activity and monoamine levels in the hippocampus of diabetic rats. These results are consistent with the previously demonstrated superiority of emoxipine and mexidol over reamberin and α-lipoic acid in the intensity of their cerebroprotective effects in alloxan-induced DM.

Effects of Oral Administration of Aspirin and Paracetamol on Plasma and Brain Protein, Tryptophan Levels and Monoamine Oxidase Activity in Rats

Effects of Oral Administration of Aspirin and Paracetamol on Plasma and Brain Protein, Tryptophan Levels and Monoamine Oxidase Activity in Rats

Effects of human placental extract on brain monoamines and monoamine oxidase activity in rats.

Human placental extract, an agent clinically used world-wide in a number of physiological anomalies, has been claimed to be effective in children of slow learners. Since the monoaminergic neurotransmitter systems in the brain play an important role in the processes of learning and memory, we examined the effects of human placental extract on the levels of norepinephrine, dopamine and serotonine in rat brain as an attempt to evaluate the possible underlying biochemical mechanism of action of the extract. We also determined the changes of brain monoamine oxidase (MAO) activity following placental extract treatment. The results showed that subchronic (5, 10, 15 or 20) administration of placental extract (2-4 ml/kg/day) had the effect of increasing all the monoamines and decreasing the MAO activity which could be the possible mode of action of the extract in slow learners.

Effects of UP 614‐04, a potential antidepressant, on cerebral monoamine oxidase activity

AbstractThe effects of UP 614‐04, a potential antidepressant agent, and those of some known antidepressant agents on cerebral monoamine oxidase (MAO) activity were compared in rats and mice. Using ex vivo and in vitro techniques, it was shown that UP 614‐04, a viloxazine analogue, inhibited cerebral MAO activity in rats and mice ex vivo, but that it was not effective in vitro. Time‐course studies revealed that the action of UP 614‐04 was more sustained than that of viloxazine, but much less potent or sustained than those of pargyline or isocarboxazide. The effect of UP 614‐04 was not selective to the A or B forms of MAO.

Studies on the effects of N,N′-dimethylformamide on ethanol disposition and on monoamine oxidase activity in rats

Pretreatment of male rats with N,N′-dimethylformamide (DMF) by oral or inhalation routes prior to ethanol administration caused marked alterations in blood ethanol and/or acetaldehyde concentrations, depending upon the DMF dose given and on the DMF-ethanol time interval. Rats were given single oral doses of DMF (2 or 20 mmol/kg or disulfiram (2 mmol/kg) and challenged with ethanol (2 g/kg po) 18 hr later. Disulfiram or DMF at equimolar doses produced peak elevations in blood acetaldehyde concentrations which were about five- and fourfold higher, respectively, than those of controls. In contrast, the 20-mmol/kg did not enhance acetaldehyde blood concentrations but resulted in approximately a twofold elevation in the peak blood ethanol concentration. Monoamine oxidase activity in brain or liver was not affected by DMF. No increases in acetaldehyde concentrations occurred when the time interval between DMF and ethanol was reduced to 3 hr. Rats were exposed to DMF by inhalation at 1000 or 6000 ppm for 3 days (4 hr/day) and given ethanol 1 hr after the last exposure. Blood acetaldehyde was increased by 46% in rats exposed to 1000 ppm of DMF when measured 30 min after ethanol. DMF exposure at 6000 ppm decreased blood acetaldehyde concentrations to 50% of control values, but increased blood ethanol concentrations by 55%. When ethanol was given 24 hr after the last DMF exposure period, marked elevations in peak blood acetaldehyde concentrations occurred at both exposure concentrations of DMF. Single oral pretreatment of rats with 2- or 20-mmol/kg doses of N-methylformamide (MF), a metabolite of DMF, 18 hr prior to ethanol also enhanced blood acetaldehyde concentrations. A similar result was obtained when rats were given 2 mmol/kg of MF only 3 hr before ethanol.

Relationships between age of submission to environmental stress, and monoamine oxidase activity in rats.

L'esposizione di giovani ratti e di ratti anziani ad uno stress cronico «ambientale» (stimolazione ottica, acustica e meccanica) ha provocato una diminuzione dell'attività monoamino ossidasica (MAO) cerebrale ed epatica. L'attività MAO si è rinormalizzata entro 7 giorni dall'ultima stimolazione, sia nei ratti giovani che nei vecchi. Viene pertanto suggerita l'assenza di differenze legate all'età, nella sensibilità delle MAO a questo tipo di stress.

Histochemical studies of the hepatic monoamine oxidase activity in rats treated with carbon tetrachloride.

Histochemical studies of the hepatic monoamine oxidase activity in rats treated with carbon tetrachloride.

HISTOCHEMICAL EVIDENCE OF MONOAMINE OXIDASE ACTIVITY IN RATS OF DIFFERENT AGES.

The histochemically detectable monoamine oxidase activity in certain organs of young and old rats is compared. Regardless of age, the activity is strong in the liver, faint in the skeletal muscle, and absent in the kidney. In the myocardium, however, the quantity of monoamine oxidase increases strongly with age. Its activity is manifest in the form of granular and diffuse formazan precipitates; both disappear after a preliminary treatment of the animals with a monoamine oxidase inhibitor. This finding indicates that the diffuse as well as the previously identified granular precipitates represent monoamine oxidase.