scholarly journals Effects of the haem precursor 5-aminolaevulinate on tryptophan metabolism and disposition in the rat

1987 ◽  
Vol 248 (1) ◽  
pp. 293-295 ◽  
Author(s):  
A A B Badawy ◽  
C J Morgan ◽  
N R Davis
Keyword(s):  
Mood Disorders ◽  
Tryptophan Metabolism ◽  
Tryptophan Pyrrolase ◽  
The Brain

5-Aminolaevulinate administration to rats inhibits cerebral 5-hydroxytryptamine synthesis by decreasing tryptophan availability to the brain secondarily to activation of hepatic tryptophan pyrrolase. The results show that tryptophan metabolism and disposition can be influenced by changes in liver haem concentration, and are discussed briefly in relation to mood disorders in the hepatic porphyrias.

scholarly journals Enhancement of rat brain tryptophan metabolism by chronic ethanol administration and possible involvement of decreased liver tryptophan pyrrolase activity

1979 ◽  
Vol 178 (3) ◽  
pp. 575-580 ◽  
Author(s):  
A A Badawy ◽  
N F Punjani ◽  
M Evans
Keyword(s):  
Methylene Blue ◽  
Rat Brain ◽  
Chronic Ethanol ◽  
Tryptophan Metabolism ◽  
Ethanol Administration ◽  
Chronic Ethanol Administration ◽  
Tryptophan Pyrrolase ◽  
Tryptophan Concentration ◽  
Phenazine Methosulphate ◽  
The Brain

1. Chronic ethanol administration enhances rat brain 5-hydroxytryptamine synthesis by increasing the availability of circulating tryptophan to the brain. This increased availability is not insulin-mediated or lipolysis-dependent. 2. Under these conditions, tryptophan accumulates in the liver and apo-(tryptophan pyrrolase) activity is completely abolished, but could be restored by administration of regenerators of liver NAD+ and/or NADP+. 3. All four regenerators used (fructose, Methylene Blue, phenazine methosulphate and sodium pyruvate) prevented the ethanol-induced increase in liver tryptophan concentration and the increased availability of tryptophan to the brain. 4. It is suggested that the enhancement of brain tryptophan metabolism by chronic ethanol administration is caused by the decreased hepatic tryptophan pyrrolase activity. The results are briefly discussed in relation to previous work with ethanol. 5. Fructose enhances the conversion of tryptophan into 5-hydroxyindol-3-ylacetic acid in brains of ethanol-treated rats, whereas Methylene Blue inhibits this conversion in both control and ethanol-treated animals.

scholarly journals The role of liver tryptophan pyrrolase in the opposite effects of chronic administration and subsequent withdrawal of drugs of dependence on rat brain tryptophan metabolism

1981 ◽  
Vol 196 (1) ◽  
pp. 161-170 ◽  
Author(s):  
A A Badawy ◽  
N F Punjani ◽  
M Evans
Keyword(s):  
Chronic Administration ◽  
Tryptophan Metabolism ◽  
Chronic Morphine ◽  
Drug Induced ◽  
Tryptophan Pyrrolase ◽  
Subsequent Withdrawal ◽  
Induced Changes ◽  
Phenazine Methosulphate ◽  
The Brain

1. Chronic administration of morphine, nicotine or phenobarbitone has previously been shown to inhibit rat liver tryptophan pyrrolase activity by increasing hepatic [NADPH], whereas subsequent withdrawal enhances pyrrolase activity by a hormonal-type mechanism. 2. It is now shown that this enhancement is associated with an increase in the concentration of serum corticosterone. 3. Chronic administration of the above drugs enhances, whereas subsequent withdrawal inhibits, brain 5-hydroxytryptamine synthesis. Under both conditions, tryptophan availability to the brain is altered in the appropriate direction. 4. The chronic drug-induced enhancement of brain tryptophan metabolism is reversed by phenazine methosulphate, whereas the withdrawal-induced inhibition is prevented by nicotinamide. 5. The chronic morphine-induced changes in liver [NADPH], pyrrolase activity, tryptophan availability to the brain and brain 5-hydroxytryptamine synthesis are all reversed by the opiate antagonist naloxone. 6. It is suggested that the opposite effects on brain tryptophan metabolism of chronic administration and subsequent withdrawal of the above drugs of dependence are mediated by the changes in liver tryptophan pyrrolase activity. 6. Similar conclusions based on similar findings have previously been made in relation to chronic administration and subsequent withdrawal of ethanol. These findings with all four drugs are briefly discussed in relation to previous work and the mechanism(s) of drug dependence.

scholarly journals Inhibition of rat brain tryptophan metabolism by ethanol withdrawal and possible involvement of the enhanced liver tryptophan pyrrolase activity

1980 ◽  
Vol 192 (2) ◽  
pp. 449-455 ◽  
Author(s):  
A A B Badawy ◽  
N F Punjani ◽  
C M Evans ◽  
M Evans
Keyword(s):  
Rat Brain ◽  
Ethanol Withdrawal ◽  
Chronic Ethanol ◽  
Tryptophan Metabolism ◽  
Ethanol Administration ◽  
Time Intervals ◽  
Chronic Ethanol Administration ◽  
Tryptophan Pyrrolase ◽  
The Brain ◽  
Withdrawal Phase

1. Chronic ethanol administration to rats was previously shown to enhance brain 5-hydroxytryptamine synthesis by increasing the availability of circulating tryptophan to the brain secondarily to the NAD(P)H-mediated inhibition of liver tryptophan pyrrolase activity. 2. At 24h after ethanol withdrawal, all the above effects were observed because liver [NAD(P)H] was still increased. By contrast, all aspects of liver and brain tryptophan metabolism were normal at 12 days after withdrawal. 3. At 7–9 days after withdrawal, brain 5-hydroxytryptamine synthesis was decreased, as was tryptophan availability to the brain. Liver tryptophan pyrrolase activity at these time-intervals was maximally enhanced. 4. Administration of nicotinamide during the withdrawal phase not only abolished the withdrawal-induced enhancement of tryptophan pyrrolase activity on day 8, but also maintained the inhibition previously caused by ethanol. Under these conditions, the withdrawal-induced decreases in brain 5-hydroxytryptamine synthesis and tryptophan availability to the brain were abolished, and both functions were enhanced. Nicotinamide alone exerted similar effects in control rats. 5. It is suggested that ethanol withdrawal inhibits brain 5-hydroxytryptamine synthesis by decreasing tryptophan availability to the brain secondarily to the enhanced liver tryptophan pyrrolase activity. 6. The results are discussed in relation to the possible involvement of 5-hydroxytryptamine in dependence on ethanol and other drugs.

scholarly journals Lack of Skeletal Muscle Serotonin Impairs Physical Performance

2021 ◽  
Vol 14 ◽  
pp. 117864692110031
Author(s):  
Marion Falabrègue ◽  
Anne-Claire Boschat ◽  
Romain Jouffroy ◽  
Marieke Derquennes ◽  
Haidar Djemai ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Endurance Training ◽  
Physical Performance ◽  
Depressive Disorders ◽  
Tryptophan Metabolism ◽  
Long Distance ◽  
Positive Effects ◽  
Tryptophan Metabolites ◽  
The Brain ◽  
Deficient Mice

Low levels of the neurotransmitter serotonin have been associated with the onset of depression. While traditional treatments include antidepressants, physical exercise has emerged as an alternative for patients with depressive disorders. Yet there remains the fundamental question of how exercise is sensed by the brain. The existence of a muscle–brain endocrine loop has been proposed: according to this scenario, exercise modulates metabolization of tryptophan into kynurenine within skeletal muscle, which in turn affects the brain, enhancing resistance to depression. But the breakdown of tryptophan into kynurenine during exercise may also alter serotonin synthesis and help limit depression. In this study, we investigated whether peripheral serotonin might play a role in muscle–brain communication permitting adaptation for endurance training. We first quantified tryptophan metabolites in the blood of 4 trained athletes before and after a long-distance trail race and correlated changes in tryptophan metabolism with physical performance. In parallel, to assess exercise capacity and endurance in trained control and peripheral serotonin–deficient mice, we used a treadmill incremental test. Peripheral serotonin–deficient mice exhibited a significant drop in physical performance despite endurance training. Brain levels of tryptophan metabolites were similar in wild-type and peripheral serotonin–deficient animals, and no products of muscle-induced tryptophan metabolism were found in the plasma or brains of peripheral serotonin–deficient mice. But mass spectrometric analyses revealed a significant decrease in levels of 5-hydroxyindoleacetic acid (5-HIAA), the main serotonin metabolite, in both the soleus and plantaris muscles, demonstrating that metabolization of tryptophan into serotonin in muscles is essential for adaptation to endurance training. In light of these findings, the breakdown of tryptophan into peripheral but not brain serotonin appears to be the rate-limiting step for muscle adaptation to endurance training. The data suggest that there is a peripheral mechanism responsible for the positive effects of exercise, and that muscles are secretory organs with autocrine-paracrine roles in which serotonin has a local effect.

Nicotine as therapeutic agent in treatment of mood disorders

2016 ◽  
Vol 33 (S1) ◽  
pp. S552-S552
Author(s):  
C. Tsopelas ◽  
N. Petros ◽  
D. Maria ◽  
P. Dimitris ◽  
G.G. Angelica ◽  
...  
Keyword(s):  
Mood Disorders ◽  
Acetylcholine Receptors ◽  
Web Search ◽  
Therapeutic Agent ◽  
Negative Attitude ◽  
Medical Databases ◽  
Positive Effects ◽  
Complex Interactions ◽  
Competing Interest ◽  
The Brain

IntroductionThe plant that has as active ingredient nicotine was chewed or smoked for many years from American natives, for its therapeutic properties. Nowadays after the extensive negative attitude towards smoking, the main provider of nicotine, researchers are now pointing out the therapeutic possibilities of nicotine in mood disorders, as a substance that is acting in the acetylcholine receptors in the brain.AimsIn this review we are trying to explore the possibilities of nicotine use as a therapeutic agent.MethodsWe did a detailed research of the main medical databases, and web search engines for relevant studies. We scrutinize them independently, before reaching consensus about appropriateness for inclusion in the study.ResultsDiadermal administration of nicotine has a positive effect in depressive disorder in 3–8 days, an effect that in one study was reversed after cessation of nicotine. Patients with depression and/or healthy subjects show improvement of attention and working memory after diadermal use of nicotine. Research is not conclusive in the sustainability of these positive affects as other researchers emphasize their short effect in mood.ConclusionNicotine presents as part of novel and promising therapeutic agents with complex interactions with other neurotransmitters in the brain. Before condemning nicotine along with smoking we should acknowledge the potential use of nicotine as a therapeutic compound since research shows that some of these positive effects appear not only to smokers after abstinence but also to non-smokers.Disclosure of interestThe authors have not supplied their declaration of competing interest.

scholarly journals Catatonia Associated With Late Paraphrenia Successfully Treated With Lithium: A Case Report

2020 ◽  
Author(s):  
Hiroko Sugawara ◽  
Junpei Takamatsu ◽  
Mamoru Hashimoto ◽  
Manabu Ikeda
Keyword(s):  
Case Report ◽  
Mood Disorders ◽  
Electroconvulsive Therapy ◽  
Late Onset ◽  
Treatment Strategies ◽  
Psychotic Symptoms ◽  
Case Presentation ◽  
Limited Efficacy ◽  
Cumulative Evidence ◽  
The Brain

Abstract Background: Catatonia is a psychomotor syndrome that presents various symptoms ranging from stupor to agitation, with prominent disturbances of volition. Its pathogenesis is poorly understood. Benzodiazepines and electroconvulsive therapy (ECT) are safe and effective standard treatments for catatonia; however, alternative treatment strategies have not been established in cases where these treatments are either ineffective or unavailable. Here, we report a case of catatonia associated with late paraphrenia classified as very-late-onset schizophrenia-like psychosis, which was successfully treated with lithium. Case presentation: A 66-year-old single man with hearing impairment developed hallucination and delusions and presented with catatonic stupor after a fall. He initially responded to benzodiazepine therapy; however, his psychotic symptoms became clinically evident and benzodiazepine provided limited efficacy. Blonanserin was ineffective, and ECT was unavailable. His catatonic and psychotic symptoms were finally relieved by lithium monotherapy.Conclusions: Catatonic symptoms are common in patients with mood disorders, suggesting that lithium may be effective in these cases. Moreover, lithium may be effective for both catatonic and psychotic symptoms, as it normalizes imbalances of excitatory and inhibitory systems in the brain, which underlies major psychosis. Cumulative evidence from further cases is needed to validate our findings.

scholarly journals Mechanistic Insights in NeuroD Potentiation of Mineralocorticoid Receptor Signaling

2019 ◽  
Vol 20 (7) ◽  
pp. 1575 ◽  
Author(s):  
Lisa van Weert ◽  
Jacobus Buurstede ◽  
Hetty Sips ◽  
Isabel Mol ◽  
Tanvi Puri ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Mood Disorders ◽  
Chromatin Remodeling ◽  
Mineralocorticoid Receptor ◽  
Protective Factor ◽  
Specific Binding ◽  
Transcription Factor Family ◽  
Direct Stimulation ◽  
The Brain ◽  
Stimulation Of

Mineralocorticoid receptor (MR)-mediated signaling in the brain has been suggested as a protective factor in the development of psychopathology, in particular mood disorders. We recently identified genomic loci at which either MR or the closely related glucocorticoid receptor (GR) binds selectively, and found members of the NeuroD transcription factor family to be specifically associated with MR-bound DNA in the rat hippocampus. We show here using forebrain-specific MR knockout mice that GR binding to MR/GR joint target loci is not affected in any major way in the absence of MR. Neurod2 binding was also independent of MR binding. Moreover, functional comparison with MyoD family members indicates that it is the chromatin remodeling aspect of NeuroD, rather than its direct stimulation of transcription, that is responsible for potentiation of MR-mediated transcription. These findings suggest that NeuroD acts in a permissive way to enhance MR-mediated transcription, and they argue against competition for DNA binding as a mechanism of MR- over GR-specific binding.

scholarly journals Hemispherical asymmetry in reports gene or protein expression related to mood disorders in the brain of rodents: A pilot systematic review

IBRO Reports ◽  
2019 ◽  
Vol 6 ◽  
pp. S477
Author(s):  
Mauricio Schuler Nin ◽  
Felipe B. Almeida ◽  
Fernanda F.S. Da Silva ◽  
Alan R. Fonseca ◽  
Carina F. Feddern ◽  
...  
Keyword(s):  
Systematic Review ◽  
Protein Expression ◽  
Mood Disorders ◽  
The Brain
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