Neuroprotective Mechanisms of Taurine in Vivo

Anderzhanova, Elmira; Saransaari, Pirjo; Oja, Simo S.

doi:10.1007/978-0-387-33504-9_42

Cited by 9 publications

(5 citation statements)

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“…This study agrees with the study by Gujral et al with rats being subjected to a working memory test [19]. The ability of animals treated with taurine to show a high level of object recognition (69.91 %) may be adduced to improved learning acquisition and memory retention by taurine [1,48,49]. It may also be that taurine influenced the activities of neurotransmitters in the brain thereby improving cognitive function [31,41].…”

Section: Discussionsupporting

confidence: 88%

Comparative Effects of Taurine and Vitamin E in Acetaminophen-Induced Oxidative Stress on Learning and Memory in Male Wistar Rats

Eze¹,

Ezekiel²,

Adams³

et al. 2018

ijSciences

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Background Stress is an integral part of human life; stressful events exert deleterious effects on normal (physiological) functions, leading to the pathogenesis of diseases. Stress alters cognition, learning, memory and emotional responses, resulting in mental disorders like depression and anxiety. The comparative effect of taurine (TAU) and vitamin E (VIT E) was evaluated on learning and memory in acetaminophen-induced oxidative stress in male Wistar rats. Methods Twenty animals weighing (100-120 g) were divided into four groups (A-D) of five rat each. Animals in Group A (control) received 0.5 ml of distilled water only while those in Group B received 100 mg/kg of acetaminophen (ACE) only. Animals in Group C received 100 mg/kg of taurine plus ACE while those in Group D received 0.5ml of Vitamin E plus ACE. The administration was done once daily for sixty days during which learning and memory of the animals were assessed using elevated plus maze and novel object recognition for rats. Results Animals in Groups A, B, C and D were able to locate the closed arm at an average of 41.0 ± 13.2 s, 67.0 ± 13.5 s, 56.3±16.6 s and 32.2± 12.1 s respectively. During the training phase, the TAU + ACE animals explored the object presented to them more (67.99 %) compared with the control and other groups. The VIT E + ACE animals have the least percentage (51.94%) in exploring the novel object that was presented to them. During the consolidation phase, the control group explored the novel object presented to them more (75.62%) when compared with the other groups. The VIT E + ACE animals have the least percentage (64.15%) in exploring the novel object that was presented to the animals. Conclusion Available evidence from this study showed that animals in acetaminophen and control groups were able to explore the elevated plus maze faster than the taurine plus acetaminophen and vitamin E plus acetaminophen groups. It also demonstrated that TAU and VIT E have protective effects on acetaminophen-associated learning and memory impairment in male rats which might be elucidated by antioxidative effects, facilitation of neurotransmitter activity and secretion of the hormone corticosterone.

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Section: Discussionsupporting

confidence: 88%

Comparative Effects of Taurine and Vitamin E in Acetaminophen-Induced Oxidative Stress on Learning and Memory in Male Wistar Rats

Eze¹,

Ezekiel²,

Adams³

et al. 2018

ijSciences

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“…Intracerebroventricular (Ahtee and Vahala, 1985) and intraperitoneal (Salimäki et al, 2003) taurine and taurine administered directly into the striatum (Ruotsalainen et al, 1998) have significantly increased extracellular dopamine . At variance, in other studies direct administration into the rat striatum did not markedly affect extracellular dopamine, but reduced extracellular dopamine metabolite dihydroxyphenylacetic acid and accentuated its NMDA-induced decrease (Anderzhanova et al, 2001(Anderzhanova et al, , 2006. Taurine inhibits the synthesis and release of serotonin in rat rostral, but not in caudal, rhombencephalic raphe cells (Becquet et al, 1993).…”

Section: Interactions With Other Transmitter Systemsmentioning

confidence: 73%

Handbook of Neurochemistry and Molecular Neurobiology

2008

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Additionally, the whole set will be available upon completion under The electronic version of the whole set will be available under The print and electronic bundle of the whole set will be available under ISBN: 978-0-387-35478-1 ß 2008 Springer Science+Business Media, LLC.All rights reserved. This work may not be translated or copied in whole or in part without the written permission of the publisher (Springer Science+Business Media, LLC., 233 Spring Street, New York, NY 10013, USA), except for brief excerpts in connection with reviews or scholarly analysis. Use in connection with any form of information storage and retrieval, electronic adaptation, computer software, or by similar or dissimilar methodology now known or hereafter developed is forbidden. The use in this publication of trade names, trademarks, service marks, and similar terms, even if they are not identified as such, is not to be taken as an expression of opinion as to whether or not they are subject to proprietary rights. springer.comPrinted on acid-free paper SPIN: 11416593 2109 -5 4 3 2 1 0 PrefaceThe brain is the organ that collects information from the environment, processes and stores the information, and generates behavior as and when needed. In essence, the brain makes us who we are. For this reason, understanding the biology of brain function is a great challenge and a major goal of modern science. The brain is one of the last great frontiers in science, and the unraveling of its mysteries is comparable in complexity to efforts in space exploration. Therefore, it was not a surprise that the U.S. Congress proclaimed the 1990s the ''Decade of the Brain,'' a movement also introduced by several other countries, thereby giving a chance for neuroscientists to focus on this topic and to have better conditions for their research.A fundamental goal of neuroscience is to understand how neurons generate behavior and the pathophysiology of different mental and neurological diseases. This requires, among other things, information about where these neurons are located, how they are connected, and how they communicate with each other in various physiological and pathophysiological conditions.At the end of the nineteenth century, the great neuroanatomist Santiago Ramon y Cajal recognized that neurons are the individual signaling elements of the brain. In this book, we focus on these nerve cells of the brain and the chemical molecules that allow them to talk to each other. The discovery of intercellular communication through endogenous molecules is a milestone in the history of science. It makes the brain a unique organ.Our aim is to describe recent discoveries about the basic operations of the brain and to provide an introduction to the adaptations for specific types of information processing. For example, at a chemical synapse, the presynaptic terminal liberates a transmitter substance that acts on the postsynaptic process. Thus, a synapse converts a presynaptic electrical signal into a chemical signal and back into a postsynaptic electrical signal.Cur...

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“…Taurine is enantiostatic, preserving near-constant tissue function in response to external perturbations, involving multiple mechanisms including modulation of intracellular calcium homeostasis, membrane stabilization, reactive radical scavenging and protection from oxidative stress [26][27][28][29]. All of these have also been implicated in the enigmatic etiology of CE development during DKA.…”

Section: Discussionmentioning

confidence: 98%

An In Vitro Paradigm for Diabetic Cerebral Oedema and its Therapy: A Critical Role for Taurine and Water Channels

et al. 2011

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The pathophysiology of cerebral oedema (CE) in diabetic ketoacidosis (DKA) remains enigmatic. We investigated the role of the idiogenic osmol taurine and aquaporin channels in an in vitro model, the SH-SY5Y neuroblastoma cell line, by sequentially mimicking DKA-like hyperglycemia/hypertonicity and hypotonic fluid therapy. Exposure to DKA-like hyperosmolarity led to shrinkage, while hypotonic fluid exposure led to cell swelling and impaired viability. Low sodium compensated in part for elevated glucose, pointing to a critical role for overall osmolality. Taurine, was synthesized and retained intracellularly during DKA-like hypertonicity, and released during hypotonicity, in part mitigating neuronal swelling. Metabolic labeling showed that the rate of taurine release was inadequate to fully prevent neuronal swelling during hypotonic fluid therapy following DKA-like hypertonicity. Under these conditions, Aquaporin4 & 9 channels were respectively down and up-regulated. Our study provides further novel insights into molecular mechanisms contributing to CE in DKA and its therapy.

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Neuroprotective Mechanisms of Taurine in Vivo

Cited by 9 publications

References 42 publications

Comparative Effects of Taurine and Vitamin E in Acetaminophen-Induced Oxidative Stress on Learning and Memory in Male Wistar Rats

Comparative Effects of Taurine and Vitamin E in Acetaminophen-Induced Oxidative Stress on Learning and Memory in Male Wistar Rats

Handbook of Neurochemistry and Molecular Neurobiology

An In Vitro Paradigm for Diabetic Cerebral Oedema and its Therapy: A Critical Role for Taurine and Water Channels

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