Long-term treatment with ammonia affects the content and release of taurine in cultured cerebellar astrocytes and granule neurons

Wysmyk, Urszula; Oja, Simo S.; Saransaari, Pirjo; Albrecht, Jan

doi:10.1016/0197-0186(94)90109-0

Cited by 18 publications

(6 citation statements)

References 37 publications

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“…In the brain, taurine occupies by quantity the 2nd place after glutamate, its concentration ranging in different species and brain regions from $3 to 9 mM (1)(2)(3)(4)(5). In cultured astrocytes, the intracellular concentration of taurine may reach 20 mM or higher (6)(7)(8)(9). Taurine has been implicated in different cell protecting and neuromodulatory functions, as well as in the CNS cell migration and development, albeit in most cases both the physiologic impacts and underlying mechanisms still await solid experimental verification.…”

Section: Introductionmentioning

confidence: 99%

Taurine Interaction with Neurotransmitter Receptors in the CNS: An Update

Albrecht

Schousboe²

2005

Neurochem Res

183

143

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Taurine appears to have multiple functions in the brain participating both in volume regulation and neurotransmission. In the latter context it may exert its actions by serving as an agonist at receptors of the GABAergic and glycinergic neurotransmitter systems. Its interaction with GABAA and GABAB receptors as well as with glycine receptors is reviewed and the physiological relevance of such interactions is evaluated. The question as to whether local extracellular concentrations of taurine are likely to reach the threshold level for the pertinent receptor populations cannot presently be answered satisfactorily. Hence more sophisticated analytical methods are warranted in order to obtain a definite answer to this important question.

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Section: Introductionmentioning

confidence: 99%

Taurine Interaction with Neurotransmitter Receptors in the CNS: An Update

Albrecht

Schousboe²

2005

Neurochem Res

183

143

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“…Of the different cell types and compartments included in the slice, astrocytes are the cells that primarily undergo swelling in a variety of hyperammonemic conditions in vivo (Ganz et al, 1989) and upon treatment with ammonia in vitro (Norenberg et al, 1991;and references therein). In cultured cerebellar astrocytes, a 24 hr treatment with a pathophysiologically relevant (1 mh4) concentration of ammonia markedly increased spontaneous release of preloaded Tau but produced no effect in cultured neurons (Wysmyk et al, 1994). Therefore, the excess of newly released Tau could originate from the astrocytic compartment.…”

Section: Discussionmentioning

confidence: 97%

Relation of taurine transport and brain edema in rats with simple hyperammonemia or liver failure

1996

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Taurine (Tau), an amino acid that abounds in brain, has been implicated in inhibitory neuromodulation and osmoregulation, the latter function being manifested by Tau release along with osmotically obligated water in response to brain tissue edema. A previous study (Hilgier and Olson: J. Neurochem. 62:197–204, 1994) had shown that simple hyperammonemia (HA) induced in rats by daily administration of ammonium acetate resulted in a decrease of both tissue specific gravity indicative of edema and Tau content, in basal ganglia (BG) but not in cerebral cortex (CC). By contrast, rats with hepatic encephalopathy (HE) following administration of a hepatotoxin, thioacetamide, were characterized by CC edema and an increased Tau content in both BG and CC. In the present study, we tested the following parameters that may potentially have affected Tau distribution in the two models: a) spontaneous, and stimulated (hypoosmolarity‐induced) release of loaded [3H] Tau in vitro from CC and BG slices; b) blood Tau content; and c) uptake of [14C] Tau in vivo from blood to brain corrected for [3H] water passage—the so‐called brain uptake index (BUI). The two edema‐affected structures: BG in the HA model and CC in the HE model, showed increased spontaneous Tau release. Edema‐associated spontaneous release of Tau may favor inhibitory neurotransmission contributing to the pathomechanism of HA or HE. Stimulated release, reflecting the ability of the tissue to reduce water content, was decreased in the BG from HA rats, in agreement with the postulated role of Tau in osmoregulation. Stimulated release was unchanged in CC of HE rats. Neither spontaneous nor stimulated release of Tau were affected in CC of HA rats or in BG of HE rats. HE, but not HA, was associated with elevated blood content and increased BUI for TAU, which in combination, contributed to the increase of Tau content in CC. The latter phenomenon adds to the list of metabolic changes distinguishing simple HA from toxic liver damage, reemphasizing the crucial role of factors other than ammonia in the pathomechanism of HE. © 1996 Wiley‐Liss, Inc.

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“…An increased spontaneous efflux of newly loaded radiolabeled TAU, possibly manifesting cell membrane leakage, was measured in slices derived from cerebral regions of hyperammonemic rats, and the increase was correlated with the tissue water content (Hilgier et al, 1996). Likewise, excessive spontanous TAU leakage was noted in cultured cerebellar astrocytes (Wysmyk et al, 1994) or rabbit Müller cells treated for 1 day with 1 mM ammonium chloride (Faff et al, 1997).…”

Section: Astrocytic Taurine: a Putative Contributor To Ammonia-inducementioning

confidence: 97%

Untitled

Albrecht

1998

Journal of Neuroscience Research

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Many neurologic disorders are related to congenital or acquired hyperammonemia (HA). Advanced symptoms of HA range from seizures in acute stages to stupor and coma in more chronic conditions, manifesting variable imbalance between the inhibitory and excitatory neurotransmission. Evidence obtained with the use of experimental HA models suggests that acute neurotoxic effects of ammonia are mediated by overactivation of ionotropic glutamate (GLU) receptors, mainly the N-methyl-D-aspartate (NMDA) receptors, and to a lesser degree the KA/AMPA receptors. NMDA receptor-mediated neurotoxicity may be potentiated by impaired control of their function by metabotropic GLU receptors, which are inactivated by ammonia. Prolonged overactivation of the NMDA receptors upon extended ammonia exposure causes their downregulation. The GLU receptor changes may be related to their excessive exposure to extrasynaptic GLU. Ammonia promotes GLU accumulation in the extrasynaptic space by enhancing its release from neurons, and/or by decreasing its reuptake to the nerve endings and astrocytes, where the effect results from inactivation (downregulation) of the astrocytic glutamate transporter GLT1. Excitotoxic effects of ammonia are augmented by increased synthesis of nitric oxide (NO), which is associated with NMDA receptor activation and/or increased synaptic transport of arginine (ARG). A shift toward neural inhibition is promoted by positive modulation of the ␥-aminobutyric acid (GABA)ergic tone resulting from excessive accumulation in the brain of endogenous central benzodiazepine receptor agonists, and from upregulation of astrocytic peripheral benzodiazepine receptors leading to elevated levels of prognenelone-derived neurosteroids, which positively modulate the GABA(A) receptor complex. Inhibitory neurotransmission may also be favored by enhanced release from astrocytes of an inhibitory amino acid, taurine.

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Long-term treatment with ammonia affects the content and release of taurine in cultured cerebellar astrocytes and granule neurons

Cited by 18 publications

References 37 publications

Taurine Interaction with Neurotransmitter Receptors in the CNS: An Update

Taurine Interaction with Neurotransmitter Receptors in the CNS: An Update

Relation of taurine transport and brain edema in rats with simple hyperammonemia or liver failure

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