Rate-limiting enzymes as targets for assessment of the brain neurotransmitter synthesis

1992 ◽  
Vol 19 (1) ◽  
pp. 124-125
Author(s):  
M Diksic ◽  
T Conway ◽  
S Rajagopal
Keyword(s):  
Brain Neurotransmitter ◽  
Neurotransmitter Synthesis ◽  
Rate Limiting ◽  
The Brain

Tryptophan hydroxylase 2 in seasonal affective disorder: underestimated perspectives?

2015 ◽  
Vol 26 (6) ◽  
Author(s):  
Alexander V. Kulikov ◽  
Nina K. Popova
Keyword(s):  
Affective Disorder ◽  
Tryptophan Hydroxylase ◽  
Seasonal Affective Disorder ◽  
Recurrent Depression ◽  
Tryptophan Hydroxylase 2 ◽  
System Functioning ◽  
Brain Neurotransmitter ◽  
The Relationship ◽  
Rate Limiting ◽  
The Brain

AbstractSeasonal affective disorder (SAD) is characterized by recurrent depression occurring generally in fall/winter. Numerous pieces of evidence indicate the association of SAD with decreased brain neurotransmitter serotonin (5-HT) system functioning. Tryptophan hydroxylase 2 (TPH2) is the key and rate-limiting enzyme in 5-HT synthesis in the brain. This paper concentrates on the relationship between TPH2 activity and mood disturbances, the association between human

scholarly journals High-fat diet-induced obesity and impairment of brain neurotransmitter pool

2020 ◽  
Vol 11 (1) ◽  
pp. 147-160
Author(s):  
Ranyah Shaker M. Labban ◽  
Hanan Alfawaz ◽  
Ahmed T. Almnaizel ◽  
Wail M. Hassan ◽  
Ramesa Shafi Bhat ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Brain Tissue ◽  
High Fat Diet ◽  
Density Lipoprotein ◽  
Obese Group ◽  
Control Group ◽  
High Fat ◽  
Brain Neurotransmitter ◽  
The Brain ◽  
Lean Group

AbstractObesity and the brain are linked since the brain can control the weight of the body through its neurotransmitters. The aim of the present study was to investigate the effect of high-fat diet (HFD)-induced obesity on brain functioning through the measurement of brain glutamate, dopamine, and serotonin metabolic pools. In the present study, two groups of rats served as subjects. Group 1 was fed a normal diet and named as the lean group. Group 2 was fed an HFD for 4 weeks and named as the obese group. Markers of oxidative stress (malondialdehyde, glutathione, glutathione-s-transferase, and vitamin C), inflammatory cytokines (interleukin [IL]-6 and IL-12), and leptin along with a lipid profile (cholesterol, triglycerides, high-density lipoprotein, and low-density lipoprotein levels) were measured in the serum. Neurotransmitters dopamine, serotonin, and glutamate were measured in brain tissue. Fecal samples were collected for observing changes in gut flora. In brain tissue, significantly high levels of dopamine and glutamate as well as significantly low levels of serotonin were found in the obese group compared to those in the lean group (P > 0.001) and were discussed in relation to the biochemical profile in the serum. It was also noted that the HFD affected bacterial gut composition in comparison to the control group with gram-positive cocci dominance in the control group compared to obese. The results of the present study confirm that obesity is linked to inflammation, oxidative stress, dyslipidemic processes, and altered brain neurotransmitter levels that can cause obesity-related neuropsychiatric complications.

scholarly journals Housing and road transport modify the brain neurotransmitter systems of pigs: Do pigs raised in different conditions cope differently with unknown environments?

PLoS ONE ◽  
2019 ◽  
Vol 14 (1) ◽  
pp. e0210406 ◽  
Author(s):  
Laura Arroyo ◽  
Daniel Valent ◽  
Ricard Carreras ◽  
Raquel Peña ◽  
Josefa Sabrià ◽  
...  
Keyword(s):  
Road Transport ◽  
Neurotransmitter Systems ◽  
Unknown Environments ◽  
Brain Neurotransmitter ◽  
The Brain

STEM-18. STROMAL EXTRACELLULAR VESICLES DRIVE GLIOMA STEM CELL REPROGRAMMING

2021 ◽  
Vol 23 (Supplement_6) ◽  
pp. vi24-vi25
Author(s):  
Lata Adnani ◽  
Brian Meehan ◽  
Jordan Kassouf ◽  
Cristiana Spinelli ◽  
Nadim Tawil ◽  
...  
Keyword(s):  
Molecular Subtype ◽  
Extracellular Vesicle ◽  
Host Cells ◽  
Tumour Mass ◽  
Membrane Structures ◽  
And Function ◽  
Rate Limiting ◽  
The Brain

Abstract Glioblastoma multiforme (GBM) represents the most frequent and lethal form of brain tumors originating from glioma stem cells (GSCs). GBM remains lethal because the rate limiting patho-mechanisms remain poorly understood. In this regard, few limitations involve the diversity 'between' cellular states and the molecular/cellular complexity 'within' the tumour mass. Using cell based- and mouse- models, we explored extracellular vesicle (EV) mediated interactions between cancer and stromal cells impacting phenotypes of GSCs as a function of their molecular subtype. EVs are spherical membrane structures that cells release to expel different molecular cargo (lipids, proteins, RNA, DNA), which can be transported across a distance in the brain and taken up by various ‘recipient’ cells resulting in reprogramming of the recipient cell's content and function. In vivo, GSCs altered their pattern of NOTCH signalling and molecular phenotype as a function of proximity to non-transformed host cells in the brain. In vitro stromal EVs altered GSC sphere forming capacity, proteome and expression of mesenchymal markers. Thus, EV mediated tumour-stromal interactions could represent a biological switch and a novel targeting point in the biology of GBM.

scholarly journals Exploring the Multi-Target Performance of Mitochondriotropic Antioxidants against the Pivotal Alzheimer’s Disease Pathophysiological Hallmarks

Molecules ◽  
2020 ◽  
Vol 25 (2) ◽  
pp. 276 ◽  
Author(s):  
Sofia Benfeito ◽  
Carlos Fernandes ◽  
Santiago Vilar ◽  
Fernando Remião ◽  
Eugenio Uriarte ◽  
...  
Keyword(s):  
Protein Misfolding ◽  
Neuronal Damage ◽  
Memory Loss ◽  
Carbon Chain ◽  
New Chemical Entities ◽  
Brain Neurotransmitter ◽  
Β Amyloid ◽  
Target Performance ◽  
Protein Misfolding And Aggregation ◽  
The Brain

Alzheimer disease (AD) is the most common neurodegenerative disease featuring progressive and degenerative neurological impairments resulting in memory loss and cognitive decline. The specific mechanisms underlying AD are still poorly understood, but it is suggested that a deficiency in the brain neurotransmitter acetylcholine, the deposition of insoluble aggregates of fibrillar β-amyloid 1–42 (Aβ42), and iron and glutamate accumulation play an important role in the disease progress. Despite the existence of approved cholinergic drugs, none of them demonstrated effectiveness in modifying disease progression. Accordingly, the development of new chemical entities acting on more than one target is attracting progressively more attention as they can tackle intricate network targets and modulate their effects. Within this endeavor, a series of mitochondriotropic antioxidants inspired on hydroxycinnamic (HCA’s) scaffold were synthesized, screened toward cholinesterases and evaluated as neuroprotectors in a differentiated human SH-SY5Y cell line. From the series, compounds 7 and 11 with a 10-carbon chain can be viewed as multi-target leads for the treatment of AD, as they act as dual and bifunctional cholinesterase inhibitors and prevent the neuronal damage caused by diverse aggressors related to protein misfolding and aggregation, iron accumulation and excitotoxicity.

A STUDY OF INTERMEDIATE CARBOHYDRATE METABOLISM IN RATS EXPOSED TO HIGH OXYGEN PRESSURES

1963 ◽  
Vol 41 (1) ◽  
pp. 327-333
Author(s):  
Ellen R. Gordon ◽  
D. O. Tinker ◽  
W. J. Watson
Keyword(s):  
Carbohydrate Metabolism ◽  
High Oxygen ◽  
Male Rats ◽  
Pasteur Effect ◽  
Glyceraldehyde Phosphate Dehydrogenase ◽  
Rate Limiting ◽  
The Brain

Exposure of male rats to 100% oxygen at 6 atmospheres for 20 minutes produced an increase in the concentration of fructose-1,6-diphosphate in the liver and muscle, but not in the brain. The activities of aldolase and glyceraldehyde phosphate dehydrogenase were measured in the liver and muscle. The change in the activity of these enzymes indicated that they had not become rate-limiting during exposure. The relation of these data to the Pasteur effect is considered.

scholarly journals Distribution of the Cystine/Glutamate Antiporter System x−c in the Brain, Kidney, and Duodenum

2006 ◽  
Vol 54 (5) ◽  
pp. 549-557 ◽  
Author(s):  
Joseph Burdo ◽  
Richard Dargusch ◽  
David Schubert
Keyword(s):  
Oxidative Stress ◽  
Vascular Endothelial Cells ◽  
Ependymal Cells ◽  
Vascular Endothelial ◽  
Specific Antibodies ◽  
Glutathione Status ◽  
Border Areas ◽  
Low Levels ◽  
Rate Limiting ◽  
The Brain

System x−c, one of the main transporters responsible for central nervous system cystine transport, is comprised of two subunits, xCT and 4F2hc. The transport of cystine into cells is rate limiting for glutathione synthesis, the major antioxidant and redox cofactor in the brain. Alterations in glutathione status are prevalent in numerous neurodegenerative diseases, emphasizing the importance of proper cystine homeostasis. However, the distribution of xCT and 4F2hc within the brain and other areas has not been described. Using specific antibodies, both xCT and 4F2hc were localized predominantly to neurons in the mouse and human brain, but some glial cells were labeled as well. Border areas between the brain proper and periphery including the vascular endothelial cells, ependymal cells, choroid plexus, and leptomeninges were also highly positive for the system x−c components. xCT and 4F2hc are also present at the brush border membranes in the kidney and duodenum. These results indicate that system x−c is likely to play a role in cellular health throughout many areas of the brain as well as other organs by maintaining intracellular cystine levels, thereby resulting in low levels of oxidative stress. (J Histochem Cytochem 54: 549–557, 2006)

Fluorescent signalling of the brain neurotransmitter γ-aminobutyric acid and related amino acid zwitterions

1996 ◽  
pp. 2191-2192 ◽  
Author(s):  
A. Prasanna de Silva ◽  
H. Q. Nimal Gunaratne ◽  
Catherine McVeigh ◽  
Glenn E. M. Maguire ◽  
Pamela R. S. Maxwell ◽  
...  
Keyword(s):  
Amino Acid ◽  
Aminobutyric Acid ◽  
Brain Neurotransmitter ◽  
The Brain ◽  
Related Amino Acid

scholarly journals Serine metabolism in the brain regulates starvation-induced sleep suppression in Drosophila melanogaster

2018 ◽  
Vol 115 (27) ◽  
pp. 7129-7134 ◽  
Author(s):  
Jun Young Sonn ◽  
Jongbin Lee ◽  
Min Kyung Sung ◽  
Hwajung Ri ◽  
Jung Kyoon Choi ◽  
...  
Keyword(s):  
Drosophila Melanogaster ◽  
Hypomorphic Mutation ◽  
Cholinergic Signaling ◽  
Sleep Behaviors ◽  
Metabolizing Enzyme ◽  
Rate Limiting ◽  
The Brain ◽  
Serine Biosynthesis ◽  
Serine Metabolism ◽  
Genetic Mutants

Sleep and metabolism are physiologically and behaviorally intertwined; however, the molecular basis for their interaction remains poorly understood. Here, we identified a serine metabolic pathway as a key mediator for starvation-induced sleep suppression. Transcriptome analyses revealed that enzymes involved in serine biosynthesis were induced upon starvation in Drosophila melanogaster brains. Genetic mutants of astray (aay), a fly homolog of the rate-limiting phosphoserine phosphatase in serine biosynthesis, displayed reduced starvation-induced sleep suppression. In contrast, a hypomorphic mutation in a serine/threonine-metabolizing enzyme, serine/threonine dehydratase (stdh), exaggerated starvation-induced sleep suppression. Analyses of double mutants indicated that aay and stdh act on the same genetic pathway to titrate serine levels in the head as well as to adjust starvation-induced sleep behaviors. RNA interference-mediated depletion of aay expression in neurons, using cholinergic Gal4 drivers, phenocopied aay mutants, while a nicotinic acetylcholine receptor antagonist selectively rescued the exaggerated starvation-induced sleep suppression in stdh mutants. Taken together, these data demonstrate that neural serine metabolism controls sleep during starvation, possibly via cholinergic signaling. We propose that animals have evolved a sleep-regulatory mechanism that reprograms amino acid metabolism for adaptive sleep behaviors in response to metabolic needs.

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