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  • 1
    Electronic Resource
    Electronic Resource
    Glutathione and Signal Transduction in the Mammalian CNS (1999)
    Oxford UK : Blackwell Science Ltd
    Journal of neurochemistry 73 (1999), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract : The tripeptide glutathione (GSH) has been thoroughly investigated in relation to its role as antioxidant and free radical scavenger. In recent years, novel actions of GSH in the nervous system have also been described, suggesting that GSH may serve additionally both as a neuromodulator and as a neurotransmitter. In the present article, we describe our studies to explore further a potential role of GSH as neuromodulator/neurotransmitter. These studies have used a combination of methods, including radioligand binding, synaptic release and uptake assays, and electrophysiological recording. We report here the characteristics of GSH binding sites, the interrelationship of GSH with the NMDA receptor, and the effects of GSH on neural activity. Our results demonstrate that GSH binds via its γ-glutamyl moiety to ionotropic glutamate receptors. At micromolar concentrations GSH displaces excitatory agonists, acting to halt their physiological actions on target neurons. At millimolar concentrations, GSH, acting through its free cysteinyl thiol group, modulates the redox site of NMDA receptors. As such modulation has been shown to increase NMDA receptor channel currents, this action may play a significant role in normal and abnormal synaptic activity. In addition, GSH in the nanomolar to micromolar range binds to at least two populations of binding sites that appear to be distinct from all known excitatory amino acid receptor subtypes. GSH bound to these sites is not displaceable by glutamatergic agonists or antagonists. These binding sites, which we believe to be distinct receptor populations, appear to recognize the cysteinyl moiety of the GSH molecule. Like NMDA receptors, the GSH binding sites possess a coagonist site(s) for allosteric modulation. Furthermore, they appear to be linked to sodium ionophores, an interpretation supported by field potential recordings in rat cerebral cortex that reveal a dose-dependent depolarization to applied GSH that is blocked by the absence of sodium but not by lowering calcium or by NMDA or (S)-2-amino-3-hydroxy-5-methyl-4-isoxazolepropionate antagonists. The present data support a reevaluation of the role of GSH in the nervous system in which GSH may be involved both directly and indirectly in synaptic transmission. A full accounting of the actions of GSH may lead to more comprehensive understanding of synaptic function in normal and disease states.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1471-4159.1999.0730889.x
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  • 2
    Electronic Resource
    Electronic Resource
    EXCHANGE OF TAURINE IN BRAIN SLICES OF ADULT and 7-DAY-OLD RATS (1971)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 18 (1971), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract— The influx or efflux of taurine in brain slices prepared from adult and 7-day-old rats was studied in Krebs-Ringer bicarbonate-glucose medium with 0,2 and 10 mm-taurine. The exchange of taurine between the slices and the medium was slow, and no steady-state concentration was reached within the experimental period of 150 min. In both experimental groups there was a net influx of taurine into the slices from 10 mm-taurine and a slight net efflux from the slices into 2 mm-taurine. The rate of influx from 10 mm-taurine was about the same in the two groups after an initial period of faster influx into the slices of adult rats. There was some rapid initial efflux into 0 and 2 mm-taurine solutions from the slices from 7-day-old rats, but with prolonged incubation these slices were better able to maintain their intracellular taurine than the slices from adult rats. The reasons and significance of the high cerebral concentration of taurine in immature brain in vivo are briefly discussed in the light of the present and earlier studies.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1971.tb09590.x
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  • 3
    Electronic Resource
    Electronic Resource
    ON THE MECHANISM OF TAURINE TRANSPORT AT BRAIN CELL MEMBRANES (1973)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 20 (1973), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: One non-saturable and two saturable transport systems were demonstrated for taurine in rat brain slices. One of the saturable systems, designated β, is characterized by a high asnity for taurine and a low transport capacity, while the other, designated ω, by a low affinity and a high transport capacity. 2,4-Dinitrophenol inhibited the saturable transport of taurine non-competitively, while hypotaurine. β-alanine, γ-aminobutyric acid, N-methyl-taurine and L-cysteic acid inhibited transport competitively. It is thus inferred that the hypothetical carrier sites of taurine at cell membrane recognize to an equal degree strongly ionized electropositive and electronegative ends of an acceptable molecule separated by two or three carbon atoms. Two is the minimal and also the optimal carbon chain length in an acceptable molecule.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1973.tb00253.x
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  • 4
    Electronic Resource
    Electronic Resource
    INCORPORATION OF PHENYLALANINE, TYROSINE AND TRYPTOPHAN INTO PROTEIN OF HOMOGENATES FROM DEVELOPING RAT BRAIN: KINETICS OF INCORPORATION AND RECIPROCAL INHIBITION (1972)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 19 (1972), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: The kinetics of the incorporation into protein of [3H]phenylalanine, [3H]tyrosine and [3H]tryptophan were studied with homogenates prepared from whole brain of 1-, 7-, 21- and 60-day-old rats. The maximal velocities (Vmax)of incorporation of phenylalanine and tyrosine decreased and the apparent Michaelis-constants (Km) for all three amino acids increased with increasing age of the rats. Tyrosine had the smallest and tryptophan the largest Km values in all age groups. Phenylalanine competitively inhibited the incorporation of tyrosine, but tyrosine inhibited non-competitively the incorporation of phenylalanine. Tryptophan inhibited competitively the incorporation of phenylalanine, but at least partially non-competitively the incorporation of tyrosine. Phenylalanine and tyrosine did not significantly affect the incorporation of tryptophan in homogenates from 60-day-old rats. In 1-day-old rats only a very large excess of phenylalanine or tyrosine inhibited detectably. The Ki for phenylalanine in the incorporation of tyrosine was significantly smaller in 1- than in 60-day-old rats. In every case the inhibition presumably occurred at a single rate-limiting step in the complicated process of incorporation of amino acids into protein.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1972.tb05116.x
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  • 5
    Electronic Resource
    Electronic Resource
    CEREBRAL PROTEINASES IN THE GROWING RAT (1970)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 17 (1970), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: —The proteolytic activity of brain homogenates obtained from 1-, 5-, 14-, 60-, 150-, and 300-day-old rats was assayed with urea-denatured haemoglobin and casein, endogenous tissue proteins, Nα-benzoyl-dl-arginine 2-naphtylamide (BANA), Nα-benzoyl-dl-arginine methyl ester (BAME), Nα-toluene p-sulphonyl-dl-arginine methyl ester (TAME), Nα-benzoyl-dl-phenylalanine 2-naphthyl ester (BPANE), and Nα-acetyl-dl-tyrosine ethyl ester (ATEE) as substrates.Several peaks of activity were detected with all these substrates in different pH ranges. Activity was highest with protein substrates at pH 3·0-4·0, with smaller peaks of activity at pH 5·5-6·5 and 8·0-9·0. At pH 3·0 the activity with trypsin substrates, viz. BANA, BAME and TAME, was also relatively high, but much less with chymotrypsin substrates, ATEE or BPANE. With BAME, TAME, BPANE and ATEE the hydrolysis rate was highest at neutral or slightly alkaline pH. During postnatal development the hydrolysis of protein substrates increased three-fold at pH 3·0 and about two-fold at pH 6·5 and 8·5. The rate of hydrolysis of BANA, BAME and TAME generally increased during the first 2 postnatal weeks and thereafter decreased, whereas no marked increase in the rate of hydrolysis of BPANE and ATEE occurred until the age of about 2 weeks. The results were less consistent with synthetic substrates than with protein substrates, indicating the existence of non-uniform alterations during development in the activity of the individual hydrolytic enzymes participating in the breakdown of brain proteins.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1970.tb02243.x
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  • 6
    Electronic Resource
    Electronic Resource
    Taurine release modified by GABAergic agents in hippocampal slices from adult and developing mice (2000)
    Springer
    Amino acids 18 (2000), S. 17-30 
    Details
    ISSN: 1438-2199
    Keywords: Keywords: Amino acids – Taurine release – GABA receptors – Hippocampal slices – Adult – Developing mouse
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary. In order to characterize the possible regulation of taurine release by GABAergic terminals, the effects of several agonists and antagonists of GABA receptors on the basal and K+-stimulated release of [3H]taurine were investigated in hippocampal slices from adult (3-month-old) and developing (7-day-old) mice using a superfusion system. Taurine release was concentration-dependently potentiated by GABA, which effect was reduced by phaclofen, saclofen and (1,2,5,6-tetrahydropyridin-4-yl)methylphosphinic acid (TPMPA) at both ages, suggesting regulation by both GABAB and GABAC receptors. The involvement of GABAA receptors could not be excluded since the antagonist bicuculline was able to affect both basal and K+-evoked taurine release. Furthermore, several GABAB receptor effectors were able to inhibit K+-stimulated taurine release in the adults, while the GABAC receptor agonists trans-4-aminocrotonic acid (TACA) and cis-4-aminocrotonic acid (CACA) potentiated this release. The potentiation of taurine release by agents acting on the three types of GABA receptors in both adult and developing hippocampus further indicates the involvement of transporters operating in an outward direction. This inference is corroborated by the moderate but significant inhibition of taurine uptake by the same compounds.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s007260050002
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  • 7
    Electronic Resource
    Electronic Resource
    Enhanced taurine release in cultured cerebellar granule cells in cell-damaging conditions (1999)
    Springer
    Amino acids 17 (1999), S. 323-334 
    Details
    ISSN: 1438-2199
    Keywords: Amino acids ; Taurine release ; Cerebellar granule cells ; Celldamaging conditions ; Glutamate receptors ; Veratridine ; Potassium stimulation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The release of taurine from cultured cerebellar granule neurons was studied in different cell-damaging conditions, including hypoxia, hypoglycemia, ischemia, oxidative stress and in the presence of free radicals. The effects of both ionotropic and metabotropic glutamate receptor agonists on the release were likewise investigated. The release of [3H]taurine from the glutamatergic granule cells was increased by K+ (50mM) and veratridine (0.1 mM), the effect of veratridine being the greater. Hypoxia and ischemia produced an initial increase in release compared to normoxia but resulted in a diminished response to K. Hypoglycemia, oxidative stress and free radicals enhanced taurine release, and subsequent K− treatment exhibited a correspondingly greater stimulation. A common feature of taurine release in all the bove conditions was a slow response to the stimulus evoked by K+ and particularly to that evoked by veratridine. All ionotropic glutamate receptor agonists potentiated taurine release, but only the action of kainate seemed to be receptor-mediated. Metabotropic receptor agonists of group I slightly stimulated the release. The prolonged taurine release seen in both normoxia and cell-damaging conditions may be of importance in maintaining homeostasis in the cerebellum and reducing excitability for a longer period than other neuroprotective mechanisms.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01361658
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  • 8
    Electronic Resource
    Electronic Resource
    Taurine and neural cell damage (2000)
    Springer
    Amino acids 19 (2000), S. 509-526 
    Details
    ISSN: 1438-2199
    Keywords: Keywords: Amino acids – Taurine – Cell-damaging conditions – Ischemia – Brain
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary. The inhibitory amino acid taurine is an osmoregulator and neuromodulator, also exerting neuroprotective actions in neural tissue. We review now the involvement of taurine in neuron-damaging conditions, including hypoxia, hypoglycemia, ischemia, oxidative stress, and the presence of free radicals, metabolic poisons and an excess of ammonia. The brain concentration of taurine is increased in several models of ischemic injury in vivo. Cell-damaging conditions which perturb the oxidative metabolism needed for active transport across cell membranes generally reduce taurine uptake in vitro, immature brain tissue being more tolerant to the lack of oxygen. In ischemia nonsaturable diffusion increases considerably. Both basal and K+-stimulated release of taurine in the hippocampus in vitro is markedly enhanced under cell-damaging conditions, ischemia, free radicals and metabolic poisons being the most potent. Hypoxia, hypoglycemia, ischemia, free radicals and oxidative stress also increase the initial basal release of taurine in cerebellar granule neurons, while the release is only moderately enhanced in hypoxia and ischemia in cerebral cortical astrocytes. The taurine release induced by ischemia is for the most part Ca2+-independent, a Ca2+-dependent mechanism being discernible only in hippocampal slices from developing mice. Moreover, a considerable portion of hippocampal taurine release in ischemia is mediated by the reversal of Na+-dependent transporters. The enhanced release in adults may comprise a swelling-induced component through Cl− channels, which is not discernible in developing mice. Excitotoxic concentrations of glutamate also potentiate taurine release in mouse hippocampal slices. The ability of ionotropic glutamate receptor agonists to evoke taurine release varies under different cell-damaging conditions, the N-methyl-D-aspartate-evoked release being clearly receptor-mediated in ischemia. Neurotoxic ammonia has been shown to provoke taurine release from different brain preparations, indicating that the ammonia-induced release may modify neuronal excitability in hyperammonic conditions. Taurine released simultaneously with an excess of excitatory amino acids in the hippocampus under ischemic and other neuron-damaging conditions may constitute an important protective mechanism against excitotoxicity, counteracting the harmful effects which lead to neuronal death. The release of taurine may prevent excitation from reaching neurotoxic levels.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s007260070003
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  • 9
    Electronic Resource
    Electronic Resource
    Hyperphenylalanaemia and the exchange of tyrosine in adult rat brain (1971)
    Springer
    Experimental brain research 14 (1971), S. 48-60 
    Details
    ISSN: 1432-1106
    Keywords: Hyperphenylalanaemia ; Tyrosine ; Blood-brain exchange ; Cerebral protein synthesis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary An account is given of an experimental design and a computing procedure for in vivo measurement of the blood-tissue exchange of amino acids and the metabolic rate of tissue proteins with radioactively labelled amino acids. The method was used for evaluation of the exchange rates of tyrosine between the plasma and the brain and between the free and protein-bound tyrosine compartments in the brain of adult rats in experimental hyperphenylalanaemia and hypertyrosinaemia. Hyperphenylalanaemia inhibited the exchange of tyrosine between plasma and brain. In both hyperphenylalanaemic and hypertyrosinaemic rats the rate of synthesis of the cerebral proteins fell. Alterations in the intracerebral pool of free amino acids produced by excessive loading with phenylalanine or tyrosine are suggested as the cause of the impairment of cerebral protein synthesis.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00234910
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  • 10
    Electronic Resource
    Electronic Resource
    Effect of electrical stimulation on the influx and efflux of taurine in brain slices of newborn and adult rats (1972)
    Springer
    Experimental brain research 15 (1972), S. 430-438 
    Details
    ISSN: 1432-1106
    Keywords: Adult and newborn rats ; Brain slices ; Taurine transport ; Electrical stimulation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Brain slices from adult and newborn rats were incubated with [35S]taurine in Krebs-Ringer bicarbonate medium at pH 7.4. In both age groups electrical stimulation increased the oxygen consumption of the slices. The influx of taurine only increased in slices from adult rats. The influx conformed to Michaelis-Menten kinetics. In slices from adult rat Vmax increased and apparent Km remained unchanged during electrical stimulation. Both Km and Vmax were greater in adult than in newborn rats. The efflux of taurine from slices depended on the intracellular concentration of taurine and was not measurably influenced by electrical stimulation.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00234128
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