Anti-Excitotoxic Actions of Taurine in the Rat Hippocampus Studied in Vivo and in Vitro

French, Edward D.; Vezzani, Annamaria; Whetsell, William O.; Schwarcz, Robert

doi:10.1007/978-1-4684-7971-3_26

Cited by 74 publications

(29 citation statements)

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“…Electrophysiological evidence indicates that taurine has hyperpolarizing effects on neurons and glia via an increase in C1 2 conductance and modulation of Ca 21 fluxes (Hanretta and Lombardini, 1987;Walz and Allen, 1987;Huxtable, 1989Huxtable, , 1992Saransaari and Oja, 1992). Taurine has been demonstrated to be a potent anticonvulsant in the CNS; indeed, taurine has protective effects in disease states such as epilepsy, hypoxia/ischemia, and excitotoxicity, all of which may be associated with excitatory amino acids (Durelli and Mutani, 1983;French et al, 1986;Schurr et al, 1987). Finally, the taurine synthetic enzyme, cysteine sulfinic acid decarboxylase, has been localized in certain cerebellar neurons and glia (Almarghini et al, 1991) and in hippocampal neurons (Taber et al, 1986;Magnusson et al, 1989).…”

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confidence: 94%

Taurine in rat posterior pituitary: Localization in astrocytes and selective release by hypoosmotic stimulation

1997

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Taurine, a gamma-aminobutyric acid (GABA)-like acidic amino acid, has previously been shown to be prominently localized to astrocytes in the supraoptic nucleus, the neurons of which contain only small amounts, and to have inhibitory actions on supraoptic neuronal activity. In the present study, taurine distribution in the neurohypophysis was determined by using a well-characterized monoclonal antibody against taurine itself. Preembedding immunohistochemistry was performed at light and electron microscopic levels by using diaminobenzidine and gold-substituted silver-intensified peroxidase (GSSP) methods. At the light microscopic level, the distribution pattern and cellular localization of taurine immunoreactivity corresponded to that of glial fibrillary acidic protein. Pituicyte cell bodies and processes displayed dense taurine immunoreactivity. Electron microscopic observations revealed strong taurine GSSP reactions in these neural lobe astrocytes, but weak taurine reactivity was seen within only some neurosecretory axons. High-performance liquid chromatography analyses demonstrated that in vitro hypoosmotic stimulation (reduction of 40 mOsm/kg) of isolated posterior pituitaries resulted in preferential increases in taurine release into the bathing medium without increased release of other amino acids. Conversely, tissue concentrations of taurine significantly decreased with hypoosmotic perfusion, while glutamate, glutamine, and GABA concentrations were not reduced. These results indicate that taurine is mainly concentrated in neurohypophysial astrocytes, which are known to engulf the neurosecretory axonal processes and terminals. Taurine released from pituicytes under basal and hypoosmotic conditions may act to suppress axon terminal depolarization and thereby depress release of neurohypophysial peptides.

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confidence: 94%

Taurine in rat posterior pituitary: Localization in astrocytes and selective release by hypoosmotic stimulation

1997

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“…Taurine is one of the most abundant free amino acids in the CNS and plays a special role in immature brain tissue. This inhibitory amino acid is known to protect neural cells from the excitotoxicity induced by excitatory amino acids and is known as an osmoregulator and neuromodulator (31)(32)(33). The extracellular concentrations of taurine have been measured by microdialysis in several animal models of ischemic injury.…”

Section: Discussionmentioning

confidence: 99%

Relationship between Cerebral Interstitial Levels of Amino Acids and Phosphorylation Potential during Secondary Energy Failure in Hypoxic-Ischemic Newborn Piglets

et al. 2004

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The aim of this study was to determine the validity of the hypothesis that excitatory amino acids are related to phosphorylation potential during primary and secondary cerebral energy failure observed in asphyxiated infants. We report here the results of experiments using newborn piglets subjected to severe transient cerebral hypoxia-ischemia followed by resuscitation. We examined cerebral energy metabolism by phosphorus nuclear magnetic resonance spectroscopy and changes in levels of amino acid neurotransmitters in the cortex by microdialysis before, during, and up to 24 h after the hypoxic-ischemic insult. The concentrations of aspartate, glutamate, taurine, and ␥-aminobutyric acid were significantly elevated during the hypoxicischemic insult compared with prebaseline values. Shortly after resuscitation, glutamate, taurine, and ␥-aminobutyric acid concentrations decreased but then began to increase again. These secondary elevations were greater than the primary elevations. A negative linear correlation was found between primary interstitial levels of glutamate and taurine and minimum values of phosphocreatine/inorganic phosphate during the secondary energy failure. The cerebral energy state depended on the time course of changes in excitatory amino acids, suggesting that amino acids play distinct roles during the early and delayed phases of injury. Abbreviations FIO 2 , fraction of inspired oxygen GABA, ␥-aminobutyric acid PCr, phosphocreatine Pi, inorganic phosphate 31 P-MRS, phosphorus nuclear magnetic resonance spectroscopy Perinatal hypoxic-ischemic encephalopathy remains a major cause of permanent neurodevelopmental disability and infant mortality (1-4). High-energy phosphate metabolites in the brains of asphyxiated infants studied by phosphorus nuclear magnetic resonance spectroscopy ( 31 P-MRS) on the first day of life showed no differences from that in normal infants. However, inverse changes in the concentrations of phosphocreatine (PCr) and inorganic phosphate (Pi) cause a significant reduction in the [PCr]/[Pi] ratio over the next several days despite optimal medical management. Low values of [PCr]/[Pi] were founded to be associated with a very poor prognosis for survival and early neurodevelopmental outcome (5, 6). The late metabolic deterioration that characterizes such infants indicates that there is chronic metabolic stress and suggests that there may be a therapeutic window in which appropriate therapy could markedly improve outcome. The origin of this secondary energy failure is probably multifactorial and related to a combination of prolonged exposure to excitatory amino acids (which initiates cellular damage mediated by Ca 2ϩ and nitric oxide), damage caused by free radicals, immunocytotoxic reactions, impairment of protein synthesis, lack of growth factors, and decreased cerebral blood flow and oxygen delivery as a result of progressive cerebral edema (7-9). Several methods for preventing secondary brain damage have been proposed (10 -15).Some animal studies using 31 P-MRS and proton magnet...

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“…[83][84][85] We hypothesized that taurine transport at the BBB is involved in the changes in taurine ISF levels under pathological conditions. We have tested TNF-a, LPS and diethyl maleate (DEM), and found that, of these compounds, TNF-a induced the uptake of taurine and mRNA expression of TAUT in TR-BBB cells (Table 2).…”

Section: Regulation Of Bbb Functions By Cns Conditionsmentioning

confidence: 99%

New Aspects of the Blood-Brain Barrier Transporters; Its Physiological Roles in the Central Nervous System

Ohtsuki

2004

Biological & Pharmaceutical Bulletin

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The blood-brain barrier (BBB) is formed by complex tight-junctions of the brain capillary endothelial cells (BCECs) and expresses various transport systems. These characteristics of the BBB make it possible to control selective transport across the BBB and to limit the non-selective brain distribution of drugs. Since understanding the mechanism of BBB transport is important for improving the BBB permeability of CNS-acting drugs, the molecular mechanism of the BBB transport has been analyzed mainly with respect to drug transport. At first, blood-to-brain influx transport was regarded as a system for transporting drugs and nutrients to the brain. This resulted in the discovery of transport systems for glucose and amino acids. 1) Subsequently, the importance of efflux transport at the BBB has been recognized after finding that P-glycoprotein (P-gp) is involved in the efflux transport of xenobiotics.2,3) Due to these studies, the BBB is now accepted as a complex transport system which is an important determinant of drug distribution to the brain.In addition to the drug permeability aspects, the physiological function of the BBB is important in the central nervous system (CNS). To date, the BBB transport system has been shown to supply nutrients, such as glucose, lactate, amino acids and nucleotides, to the brain. However, it is conceivable that the BBB have many other physiological functions involving regulation of the CNS milieu. For instance, the brain is a highly energy-consuming tissue and produces various metabolites. In particular, metabolism is essential for the inactivation of neurotransmitters after their secretion from the pre-synapses, as well as re-uptake. The metabolites produced in the brain must be removed in order to maintaine proper neural function. Therefore, the BBB can be thought to act as a clearance system to remove various metabolites from the CNS.Clarifying the physiological role of the BBB is also necessary to understand the role of the BBB in CNS disorders. This is because an alteration in BBB functions may result in a change in CNS conditions leading to CNS disorders. Furthermore, analyzing the BBB functions from a different point of view could result in the discovery of a new transport system that is involved in drug permeability. In this review, I shall introduce the recent advances in research into the molecular basis of BBB transport, focusing on its physiological functions.The BBB Supplies Creation to the Brain The brain consumes 18% of total body energy, while its weight is only 2% of the total body weight. The brain cannot store glucose for energy synthesis, and the BBB plays a crucial role in glucose supply to the brain by expressing glucose transporter 1 (GLUT1) (Fig. 1). 4) Besides energy synthesis, an energystoring system is necessary for maintain energy homeostasis in high energy-consuming tissues. We have shown that the BBB also plays an important role in the energy storing process (Fig. 1). 5)Creatine plays a key role in this energy-storing process. The phosphate-bound energy...

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Anti-Excitotoxic Actions of Taurine in the Rat Hippocampus Studied in Vivo and in Vitro

Cited by 74 publications

References 38 publications

Taurine in rat posterior pituitary: Localization in astrocytes and selective release by hypoosmotic stimulation

Taurine in rat posterior pituitary: Localization in astrocytes and selective release by hypoosmotic stimulation

Relationship between Cerebral Interstitial Levels of Amino Acids and Phosphorylation Potential during Secondary Energy Failure in Hypoxic-Ischemic Newborn Piglets

New Aspects of the Blood-Brain Barrier Transporters; Its Physiological Roles in the Central Nervous System

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