Hormonal Action on Monoamine Oxidase Activity in Rats

Ho-Van-Hap, A.; Babineau, L. M.; Berlinguet, Louis

doi:10.1139/o67-042

Cited by 41 publications

(17 citation statements)

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“…Although there is no direct evidence for such an effect, modulation of membrane potential in other neuronal populations by glucocoticoids has been reported and these effects, consistently with our findings, depend on background electrical activity (9). Second, glucocorticoids may decrease dopamine catabolism by acting as a reversible monoamino oxidase inhibitor (23)(24)(25). This effect is consistent with the fact that administration of synthetic glucocorticoids decreases deaminated products of dopamine, such as HVA and DOPAC (25,26), that depend on monoamino oxidase activity, while increasing 3MT levels (25).…”

Section: Discussionsupporting

confidence: 79%

“…Glucocorticoids share the neurochemical actions of psychostimulants in that they both increase extracellular concentrations of dopamine (this paper) and both seem to exert this effect through inhibition of dopamine reuptake and inhibition of monoamino oxidase activity (23)(24)(25)(26)(27)(28)(29). At the behavioral level, corticosterone induces self-administration (19) and dopamine-dependent locomotor activity as do psychostimulants (30).…”

Section: Discussionmentioning

confidence: 86%

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Glucocorticoids have state-dependent stimulant effects on the mesencephalic dopaminergic transmission.

Piazza

Rougé‐Pont

Deroche

et al. 1996

Proc. Natl. Acad. Sci. U.S.A.

306

185

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An increase in the activity of mesencephalic dopaminergic neurons has been implicated in the appearance of pathological behaviors such as psychosis and drug abuse. Several observations suggest that glucocorticoids might contribute to such an increase in dopaminergic activity. The present experiments therefore analyzed the effects of corticosterone, the major glucocorticoid in the rat, both on dopamine release in the nucleus accumbens of freely moving animals by means of microdialysis, and on locomotor activity, a behavior dependent on accumbens dopamine. Given that glucocorticoids have certain state-dependent neuronal effects, their action on dopamine was studied in situations differing in dopaminergic tonus, including during the light and dark phases of the circadian cycle, during eating, and in groups of animals differing in their locomotor reactivity to novelty. Dopaminergic activity is increased in the dark period, further increased during food-intake, and is higher in rats defined as high responders to novelty than in low responders. Corticosterone, peripherally administered in a dose that approximates stress-induced plasma concentrations, increased extracellular concentrations of dopamine, and this increase was augmented in the dark phase, during eating, and in high responder rats. Corticosterone had little or no effects in the light phase and in low responder rats. Corticosterone also stimulated locomotor activity, an effect that paralleled the release of dopamine and was abolished by neurochemical (6-hydroxydopamine) depletion of accumbens dopamine. In conclusion, glucocorticoids have state-dependent stimulant effects on mesencephalic dopaminergic transmission, and an interaction between these two factors might be involved in the appearance of behavioral disturbances.It is generally admitted that an increase in the activity of the mesencephalic dopaminergic (DA) neurons is related to the appearance of pathological behaviors. The major antipsychotic drugs are antagonists of DA receptors (1) and prolonged use of psychotropic compounds known to increase DA activity can induce psychotic symptoms (2). Furthermore, an enhanced DA activity in the nucleus accumbens is associated with an increased vulnerability to develop drug self-administration in laboratory rats (3).Indirect observations suggest that glucocorticoids, the final product of the activation of the hypothalamus-pituitaryadrenal axis by stress, might be one factor capable of increasing the activity of mesencephalic DA neurons. DA neurons express corticosteroid receptors (4) and dopamine-mediated behaviors are profoundly facilitated by glucocorticoids (5). Furthermore, increased glucocorticoid levels can induce behavioral changes similar to those attributed to enhanced DA activity. In humans, high levels of glucocorticoids can induce mood changes ranging from euphoria to psychosis (6, 7). In animals, glucocorticoids, within the range of stressor-induced plasma concentrations, increase the propensity to develop self-administration of drugs of a...

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Section: Discussionsupporting

confidence: 79%

Section: Discussionmentioning

confidence: 86%

Glucocorticoids have state-dependent stimulant effects on the mesencephalic dopaminergic transmission.

Piazza

Rougé‐Pont

Deroche

et al. 1996

Proc. Natl. Acad. Sci. U.S.A.

306

185

View full text Add to dashboard Cite

show abstract

“…Effects of corticosterone on TH have been demonstrated in the locus coeruleus (24), hypothalamus (25), and more recently in the VTA (26), though important individual differences in the latter effects have been reported (26). Second, glucocorticoids may decrease dopamine catabolism acting as reversible monoamine oxidase inhibitors (27)(28)(29). This action of glucocorticoids is consistent with the fact that dexamethasone decreases deaminated products of dopamine such as HVA and DOPAC (29,30), which depend on monoamine oxidase activity, whereas it increases 3MT levels that depend on COMT (catechol-O-methyltransferase) (29).…”

Section: Discussionmentioning

confidence: 99%

Suppression of glucocorticoid secretion and antipsychotic drugs have similar effects on the mesolimbic dopaminergic transmission

Piazza

Barrot

Rougé‐Pont

et al. 1996

Proc. Natl. Acad. Sci. U.S.A.

112

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Specific antagonists of central dopaminergic receptors constitute the major class of antipsychotic drugs (APD). Two principal effects of APD are used as criteria for the pre-clinical screening of their antipsychotic action: (i) inhibition of basal and depolarization-induced activity of mesolimbic dopaminergic neurons; (ii) antagonism of the locomotor effects of dopaminergic agonists. Given that glucocorticoid hormones in animals increase dopamine release and dopamine-mediated behaviors and that high levels of glucocorticoids can induce psychotic symptoms in humans, these experiments examined whether inhibition of endogenous glucocorticoids might have APD-like effects on mesolimbic dopaminergic transmission in rats. It is shown that suppression of glucocorticoid secretion by adrenalectomy profoundly decreased (by greater than 50%): (i) basal dopaminergic release and the release of dopamine induced by a depolarizing stimulus such as morphine (2 mg͞kg, s.c.), as measured in the nucleus accumbens of freely moving animals by microdialysis; (ii) the locomotor activity induced by the direct dopaminergic agonist apomorphine. The effects of adrenalectomy were glucocorticoid specific given that they were reversed by the administration of glucocorticoids at doses within the physiological range. Despite its profound diminution of dopaminergic neurotransmission, adrenalectomy neither modified the number of mesencephalic dopaminergic neurons nor induced gliosis in the mesencephalon or in the nucleus accumbens, as shown by tyrosine hydroxylase and glial fibrillary acidic protein immunostaining. In conclusion, these findings suggest that blockade of central effects of glucocorticoids might open new therapeutic strategies of behavioral disturbances.The discovery of treatments reducing the activity of the central dopaminergic (DA) transmission is one of the main goals of neuroscience and pharmacological researches. Interest in dopamine has been sustained by the discovery that antipsychotic drugs (APD) were potent antagonists of the DA receptors (1). Decades of intensive research has considerably enlarged our knowledge about the functional role of DA neurons (2), suggesting that their hyperactivity may be involved in various behavioral pathologies, such as psychosis and addiction (3, 4). Nevertheless, antagonists of DA receptors are still the only class of drugs used in clinical practice to antagonize DA activity.There is evidence indicating that glucocorticoid hormones may be one of the factors determining a pathological hyperactivity of DA neurons. First, an increase in glucocorticoids can induce behavioral changes that are among those attributed to the enhancement of DA activity. For example, high levels of glucocorticoids can generate mood changes ranging from euphoria to psychosis in humans (5, 6), and increase the propensity to develop self-administration of drugs of abuse in animals (7). Second, administration of glucocorticoids increases extracellular concentrations of dopamine in vivo (8) and in vitro (9) and faci...

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“…cardiac MAO activity was increased in hyper thyroid rats or by administration of thyro mimetic compounds (10, 13,14). However, in this study, it was confirmed that MAO activity in heart, lung and liver mitochondria decreased repidly to about 50% that of the control values on the first days; and after that, heart MAO activity increased gradually and completely restored to the control value after 10 days, although it has been reported that there is a continous increase of cardiac MAO activity with age and weight in male rats up to 16 weeks of age (10, 18).…”

Section: Discussionmentioning

confidence: 99%

“…In contrast, there have been reports which show an increase of hepatic MAO activity by in thyroid-fed rats (11) and no measurable change in myocardiac MAO activity following administration of thyromimetic compounds (12). However, these discrepancies in the measurements of MAO activity depend on the sex and age of the animals used (7, 10, 13,14).…”

mentioning

confidence: 99%

Changes in MAO activities in several organs of rats after administration of l-thyroxine.

Egashira

Yamanaka

1987

Jpn.J.Pharmacol

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Abstract-Male rats were given daily injections of 200 /eg/kg /-thyroxine, s.c., for a period of 10 days. Monoamine oxidase (MAO) activities in the heart, lung and liver mitochondria decreased rapidly to about 50% those of the control rats with 5-HT and i3-phenylethylamine (13-PEA) as substrates on the first day. After that, heart MAO activity increased gradually and exceeded the control value after 10 days with 5-HT as the substrate. The level of liver MAO activity was maintained at about 50-70% during the same period of administration with 5-HT as the substrate. The thyroxine treated rats showed no marked change in brain MAO activity. In vitro, /-thyroxine and its metabolites had no discriminative actions on MAO activities in these organs of rats. The heart, lung and liver MAO have unaltered Km values for 5-HT and (3-PEA, but decreases in the Vm87z for both substrates were observed be tween the control and /-thyroxine-treated rats. Addition of the brain, heart and

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Hormonal Action on Monoamine Oxidase Activity in Rats

Cited by 41 publications

References 0 publications

Glucocorticoids have state-dependent stimulant effects on the mesencephalic dopaminergic transmission.

Glucocorticoids have state-dependent stimulant effects on the mesencephalic dopaminergic transmission.

Suppression of glucocorticoid secretion and antipsychotic drugs have similar effects on the mesolimbic dopaminergic transmission

Changes in MAO activities in several organs of rats after administration of l-thyroxine.

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