The role of tryptophan in hepatic encephalopathy

1993 ◽  
Vol 5 (4) ◽  
pp. 71-75
Author(s):  
C. Aaldijk ◽  
W.W. Van Den Broek ◽  
R.C. Van Der Mast
Keyword(s):  
Hepatic Encephalopathy ◽  
Clinical Picture ◽  
Serotonergic System ◽  
Pathogenetic Mechanisms ◽  
Research Findings ◽  
Glutamine Synthesis ◽  
The Brain ◽  
Tryptophan Uptake

SummaryIn this review the most important hypotheses for the occurrence of the clinical picture of hepatic encephalopathy are discussed. As possible pathogenetic mechanisms are raised: dysfunction of the serotonergic system due to an increased tryptophan uptake in the brain, an elevated intracerebral ammoniac concentration and glutamine synthesis, and a heightened intracerebral GABA-activity.The dysregulation of the serotonergic system as a consequence of the increased intracerebral tryptophan uptake is described as one of the most important pathogenetic mechanisms. The elevated intracerebral ammoniac concentration and the elevated intracerebral glutamine synthesis play in this a facilitating role. The similarity in symptomatology of the clinical picture of HE and the serotonergic syndrome support this hypothesis. Due to contradictory research findings the role of the GABA-ergic system and the occurrence of HE remains unclear.

scholarly journals Affective spectrum disorders and role of serotonergic system of the brain

2014 ◽  
Vol 1 (3) ◽  
pp. 168-173
Author(s):  
Ivana Timotijevic ◽  
Mirjana Todorovic ◽  
Katarina Crnic ◽  
Srdjan Markovic ◽  
Dragana Kastratovic
Keyword(s):  
Serotonergic System ◽  
Spectrum Disorders ◽  
The Brain

Understanding as Living

2019 ◽  
pp. 7-53
Author(s):  
James W. Jones
Keyword(s):  
Sensory Experience ◽  
Laboratory Research ◽  
Interactive System ◽  
The World ◽  
Human Understanding ◽  
Research Findings ◽  
Network Studies ◽  
The Brain ◽  
Religious Understanding

Drawing upon clinical psychoanalysis and laboratory research, this chapter develops an “embodied-relational” epistemology. The chapter reviews major research findings on the ways embodiment influences the cognitive processes by which we understand ourselves and the world. It also reviews current neuro-network studies whose findings imply the brain can be understood as a single, interactive system and not simply a collection of relatively autonomous domains. The emphasis here is on the brain’s complexity, integration, and a certain degree of openness. Sensory experience is understood as an active, not passive process, involving an intimate interconnection between self and world. The role of proprioception, as well as the five basic senses, is analyzed. The implications of such research findings for human understanding, and especially religious understanding, are elaborated.

scholarly journals Genetic approaches to the investigation of serotonergic neuron functions in animals

2019 ◽  
Vol 23 (4) ◽  
pp. 448-455
Author(s):  
U. S. Drozd ◽  
E. V. Shaburova ◽  
N. N. Dygalo
Keyword(s):  
Developmental Stages ◽  
Sensory Information ◽  
Serotonergic System ◽  
Serotonergic Neurons ◽  
Neurotransmitter Systems ◽  
New Therapeutic Approaches ◽  
Serotonin System ◽  
The Brain

The serotonergic system is one of the most important neurotransmitter systems that take part in the regulation of vital CNS functions. The understanding of its mechanisms will help scientists create new therapeutic approaches to the treatment of mental and neurodegenerative diseases and find out how this neurotransmitter system interacts with other parts of the brain and regulates their activity. Since the serotonergic system anatomy and functionality are heterogeneous and complex, the best tools for studying them are based on manipulation of individual types of neurons without affecting neurons of other neurotransmitter systems. The selective cell control is possible due to the genetic determinism of their functions. Proteins that determine the uniqueness of the cell type are expressed under the regulation of cell-specific promoters. By using promoters that are specific for genes of the serotonin system, one can control the expression of a gene of interest in serotonergic neurons. Here we review approaches based on such promoters. The genetic models to be discussed in the article have already shed the light on the role of the serotonergic system in modulating behavior and processing sensory information. In particular, genetic knockouts of serotonin genes sert, pet1, and tph2 promoted the determination of their contribution to the development and functioning of the brain. In addition, the review describes inducible models that allow gene expression to be controlled at various developmental stages. Finally, the application of these genetic approaches in optogenetics and chemogenetics provided a new resource for studying the functions, discharge activity, and signal transduction of serotonergic neurons. Nevertheless, the advantages and limitations of the discussed genetic approaches should be taken into consideration in the course of creating models of pathological conditions and developing pharmacological treatments for their correction.

scholarly journals Is the role of melatonin in induction of ovulation in the light-induced constant estrous anovulatory state mediated through the brain serotonergic system ?

1980 ◽  
Vol 20 (6) ◽  
pp. 1893-1898 ◽  
Author(s):  
Carmela F DE GAETANI ◽  
Rosanna POGGIOLI ◽  
Paola FERRARI ◽  
B. MESS ◽  
G. P. TRENTINI
Keyword(s):  
Serotonergic System ◽  
Induction Of Ovulation ◽  
The Brain

Newer aspects of glutamine/glutamate metabolism: the role of acute pH changes

1999 ◽  
Vol 277 (4) ◽  
pp. F493-F497 ◽  
Author(s):  
Itzhak Nissim
Keyword(s):  
Glutamate Metabolism ◽  
Oxidative Deamination ◽  
Carbamyl Phosphate ◽  
Ph Changes ◽  
Extracellular Compartment ◽  
Neuronal Metabolism ◽  
Glutamine Synthesis ◽  
Kidney Liver ◽  
The Brain

This review focuses on the role of acute pH changes in the regulation of Gln/Glu metabolism in the kidney, liver, and brain. Alterations of proton concentration ([H+]) profoundly affect flux through phosphate-dependent glutaminase (PDG) or glutamate dehydrogenase (GDH), the primary enzymes responsible for mitochondrial metabolism of glutamine and glutamate, respectively. In the kidney, acute acidosis stimulates Gln uptake and its metabolism via the PDG pathway. The Glu formed from Gln can be removed via 1) oxidative deamination through the GDH reaction, 2) transamination reactions, and 3) transport of Glu from intracellular to extracellular compartment, thereby diminishing the intramitochondrial pool of glutamate sufficiently to stimulate flux through the PDG pathway. Converse changes may occur with increased pH. In the liver, acidosis diminishes the rate of Gln and Glu metabolism via the PDG and GDH pathways, but stimulates glutamine synthesis (i.e., glutamine recycling). Alkalosis has little effect. Hepatic Gln metabolism via the PDG pathway has a central role in ureagenesis via 1) supplementation of nitrogen for the synthesis of carbamyl phosphate, and 2) providing glutamate for N-acetylglutamate synthesis. In the brain, Gln/Glu metabolism links ammonia detoxification and energy metabolism via 1) detoxification of ammonia and excess glutamate by glutamine synthesis in astrocytes, 2) formation and export of glutamine to neurons where it is metabolized to glutamate and GABA, and 3) production of α-ketoglutarate and lactate from Glu and their transport to neurons. Changes in intracellular pH associated with changes in cellular [K+] may have a key role in the regulation of these processes of glial-neuronal metabolism of Gln/Glu metabolism.

Suicide, Serotonin, and the Brain

Crisis ◽  
2001 ◽  
Vol 22 (2) ◽  
pp. 66-70 ◽  
Author(s):  
C. van Heeringen
Keyword(s):  
Suicidal Behavior ◽  
Behavioral Inhibition ◽  
Biological Psychiatry ◽  
Future Research ◽  
Research Findings ◽  
The Central Nervous System ◽  
Serotonergic Function ◽  
The Brain ◽  
Serotonergic Dysfunction

Summary: The involvement of impaired serotonergic functioning in the development of suicidal behavior is one of the best documented findings in biological psychiatry. It is, however, less clear in which way this dysfunction contributes to the occurrence of suicidal behavior. Correlational studies have demonstrated associations between peripheral measures of serotonergic function and characteristics such as impulsivity, disinhibition, anxiety, and/or behavioral inhibition. Postmortem and neuroimaging studies have provided insight in the localization of serotonergic dysfunction in the central nervous system. Nevertheless, results in this area of research have also been contradictory. Following a short overview of recent research findings on serotonin and suicidal behavior, this paper focuses on the involvement of the prefrontal cortex of the brain in the development of suicidal behavior and on the role of serotonin in its executive functions. Based on these considerations, suggestions for future research are discussed.

scholarly journals Toxic encephalopathy in a clinicl case of polycythemia vera

2020 ◽  
Vol 18 (4) ◽  
pp. 249-255
Author(s):  
P. I. Kuznetsova ◽  
M. M. Tanashyan ◽  
A. A. Kornilova
Keyword(s):  
Hepatic Encephalopathy ◽  
Cerebrovascular Disorders ◽  
Toxic Encephalopathy ◽  
Vein Thrombosis ◽  
Toxic Damage ◽  
Myeloproliferative Diseases ◽  
Paramagnetic Substance ◽  
The Relationship ◽  
The Brain

The article deals with a clinical case description of a female patient with toxic encephalopathy against the background of Ph-negative myeloproliferative diseases. The article discusses symptoms and neuroimaging of hepatic encephalopathy developed as a result of a shunt placed after portal vein thrombosis. The issues of etiology and pathogenesis of hepatic encephalopathy, principles of therapy, as well as the unique clinical picture of nervous system damage in this condition are also discussed. Data on the role of manganese in development of toxic encephalopathy, accumulation of paramagnetic substance in the basal ganglia of the brain and development of extrapyramidal symptoms are presented. The pathogenesis of toxic damage to neurons, increase in their sensitivity to hypoxia, and the relationship with the risk of cerebrovascular disorders and development of chronic cerebral ischemia, contributing to reduction of cognitive functions, are described.

CNS Arousal Systems: Possible Role in Delirium

1991 ◽  
Vol 3 (2) ◽  
pp. 353-371 ◽  
Author(s):  
Christopher A. Ross
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cerebral Cortex ◽  
Hepatic Encephalopathy ◽  
Cholinergic Neurons ◽  
Cholinergic Systems ◽  
Normal Sleep ◽  
New Research ◽  
The Brain

Delirium is often considered a global and nonspecific alteration in cerebral function. However, the recent clinical evidence for heterogeneity within the syndrome of delirium suggests that different systems of the brain may be important in different kinds of delirium. Some forms of delirium, such as anticholinergic toxicity and hepatic encephalopathy, may be caused by drugs or toxins acting on specific brain neurochemical systems. The neurophysiological bases of the control of normal arousal and attention are still relatively poorly understood. However, the recent appreciation of the existence of neurotransmitter-specific projections from the hypothalamus and brain stem directly to the cerebral cortex has spurred new research. Some of these projections may be important in particular kinds of delirium; for instance, evidence from a number of different lines of research implicates GABA systems in the brain as being important in the delirium of hepatic encephalopathy. Cholinergic neurons in the basal forebrain and pons innervate the cerebral cortex. Both of these neurons, but particularly the pontine group, may be important in the delirium of anticholinergic toxicity. Thus, more research on the physiology of these systems in normal sleep and arousal, as well as in pathophysiological states, is indicated. Little is known about changes in these systems with aging. The well-known degeneration in cholinergic systems in Alzheimer's disease, and the sensitivity of individuals with Alzheimer's disease to anticholinergic toxicity, suggest a role of central cholinergic systems in anticholinergic delirium in demented patients. Further research into the involvement of the other systems in aging and delirium apparently would be fruitful.

Neuropeptides and anxiety disorders

1992 ◽  
Vol 4 (2) ◽  
pp. 25-30 ◽  
Author(s):  
H.J.G.M. van Megen ◽  
J.A. den Boer ◽  
H.G.M. Westenberg
Keyword(s):  
Anxiety Disorders ◽  
Animal Experiments ◽  
Future Research ◽  
Working Mechanism ◽  
Animal Data ◽  
Research Findings ◽  
Relationship Of ◽  
The Relationship ◽  
The Brain

SummaryIn this review article four neuropeptides: adrenocorticotrope hormone (ACTH), corticotrope releasing hormone (CRH), neuropeptide- Y(NPY) and cholecystokinin (CCK) are discussed with respect to their possible role in the pathogenesis of anxiety disorders. First the presumable working mechanism of these peptides in the brain is mentioned. In addition, the relationship of these peptides and anxiety is outlined using neuroanatomical and electrophysiological research data. Subsequently, animal experiments and human research findings are discussed. Most of the research findings so far are obtained from animal data. Only with respect to CCK, there is increasing evidence, also from human studies, that this peptide might play a role in the pathogenesis of anxiety disorders. The putative role of the other peptides remains to be estab lished in future research.

scholarly journals Gut Microbes and Hepatic Encephalopathy: From the Old Concepts to New Perspectives

2021 ◽  
Vol 9 ◽  
Author(s):  
Alba Rocco ◽  
Costantino Sgamato ◽  
Debora Compare ◽  
Pietro Coccoli ◽  
Olga Maria Nardone ◽  
...  
Keyword(s):  
Hepatic Encephalopathy ◽  
Metabolic Pathways ◽  
Treatment Strategies ◽  
Advanced Liver Disease ◽  
Gut Microbes ◽  
Novel Treatment ◽  
Research Findings ◽  
Novel Treatment Strategies

Hepatic encephalopathy (HE) is a severe complication of advanced liver disease and acute liver failure. The clinical spectrum ranges from minor cognitive dysfunctions to lethargy, depressed consciousness, and coma and significantly impact the quality of life, morbidity, and mortality of the patients. It is commonly accepted that the gut milieu is essential for the development of HE; however, despite intensive research efforts, the pathogenesis of HE is still not fully elucidated. As our knowledge of gut microbiota moves from the pioneering era of culture-dependent studies, the connection between microbes, inflammation, and metabolic pathways in the pathogenesis of HE is becoming increasingly clear, providing exciting therapeutic perspectives. This review will critically examine the latest research findings on the role of gut microbes in the pathophysiological pathways underlying HE. Moreover, currently available therapeutic options and novel treatment strategies are discussed.

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