Ammonia-induced taurine release from cultured rabbit m�ller cells is an osmoresistant process mediated by intracellular accumulation of cyclic AMP

Faff, Lidia; Reichenbach, Andreas; Albrecht, Jan

doi:10.1002/(sici)1097-4547(19961015)46:2<231::aid-jnr11>3.0.co;2-5

Cited by 23 publications

(9 citation statements)

References 23 publications

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“…Stimulation of NMDA receptors, which is the trigger of glutamate neurotoxicity, evokes taurine release to the extracellular space (15,18,65,66). Ammonia, which can exert its neurotoxic action by overactivating NMDA receptors among other mechanisms, likewise stimulates taurine release in vivo by an NMDA receptor-mediated mechanism (20,67,68), whereby acute ammonia challenge appears to release taurine more readily than any other amino acid studied (20,(69)(70)(71)(72)(73).…”

Section: Taurine Interaction With Gaba a Receptorssupporting

confidence: 93%

Taurine Interaction with Neurotransmitter Receptors in the CNS: An Update

Albrecht

Schousboe²

2005

Neurochem Res

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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: Taurine Interaction With Gaba a Receptorssupporting

confidence: 93%

Taurine Interaction with Neurotransmitter Receptors in the CNS: An Update

Albrecht

Schousboe²

2005

Neurochem Res

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183

143

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“…Hyperammonemia is associated with cerebral edema resulting from astrocytic swelling (27, and references therein), which is thought to be partly responsible for the increased taurine efflux (21). However, studies with cultured glial cells revealed distinct features of ammonia-induced efflux as compared to hypoosmolarity or high potassium-induced efflux: partial chloride-independence (12), resistance to changes of osmolarity and chloride channel inhibitors and dependence on cAMP (11,24). Moreover, chronic treatment with ammonia in vitro that does not affect cell volume likewise increased taurine efflux from cultured glial cells (25,26), and it did so in a cAMP-dependent, osmoresistant manner (25).…”

Section: Introductionsupporting

confidence: 92%

“…Hyperammonemia leads to taurine accumulation in the extrasynaptic space in vivo (18)(19)(20)(21)(22), an effect held responsible for increased neural inhibition and/or neuroprotection (23). Ammonia is among the most potent triggers of taurine efflux from astrocytes (11,12,(24)(25)(26). Hyperammonemia is associated with cerebral edema resulting from astrocytic swelling (27, and references therein), which is thought to be partly responsible for the increased taurine efflux (21).…”

Section: Introductionmentioning

confidence: 99%

The Role of Protein Kinase C and Cyclic AMP in the Ammonia-Induced Shift of the Taurine Uptake/Efflux Balance Towards Efflux in C6 Cells

2005

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A previous study showed that treatment of C6 glioma cells with 10 mM ammonium chloride monia") for 24 h decreases taurine uptake and evokes sodium-dependent taurine efflux, indicating reversal of the taurine transporter (TauT)-mediated transport as an underlying mechanism. Consistent with the involvement of TauT we now show that the ammonia-induced changes in Tau uptake and efflux are inhibited by the protein kinase C (PKC) activator phorbol 12,13-dibutyrate (PDBu). Ammonia treatment of C6 cells resulted in increased intracellular accumulation of cAMP. Incubation of the cells with dibutyryl cAMP (dbcAMP) mimicked the effects of ammonia on both taurine uptake and efflux. The effects of dbcAMP on taurine uptake and efflux were additive to the effects of ammonia. Collectively, the results suggest that the effects of ammonia on taurine uptake and efflux may be partly mediated by cAMP. Consistent with this mechanism, the adenyl cyclase inhibitor, miconazole reduced the stimulation of efflux by ammonia.

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“…These results suggest that NO and cGMP play a significant role in the NH 3 -mediated positive inotropic effect. Our results are consistent with those of a previous report by Faff et al (Faff et al, 1996), who proposed that NH 3 might act in cell signaling through activation of cAMP-dependent signaling pathways in which mildly increased cGMP inhibits cAMP hydrolysis through inhibition of phosphodiesterase.…”

Section: Discussionmentioning

confidence: 99%

The inotropic effects of ammonia on isolated perfused rat hearts and the mechanisms involved

Zhang

Meng

2011

Journal of Experimental Biology

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SUMMARYAmmonia (NH 3 ) is a common exogenous gas in the atmosphere, as well as an endogenous chemical produced by amino acid catabolism and other pathways in vivo. Physiological and pathophysiological roles of NH 3 in the nervous system have been studied. Recently, endogenous NH 3 has been suggested to be a gas transmitter. However, so far the role of NH 3 in cardiovascular functions has not been reported. The present study was designed to investigate the inotropic effects of NH 3 on isolated perfused rat hearts and the possible mechanisms involved in these effects. The results showed that NH 3 had a positive inotropic effect in a concentration-dependent manner and produced a higher positive effect than NaOH and NH 4 Cl. At low concentrations, the effect of NH 3 on cardiac function was caused by NH 3 molecules; at high concentrations, the effect of NH 3 on hearts may be partly correlated with a change of pH value, but was mainly caused by NH 3 molecules. The mechanisms involved in the NH 3 -ATPase in the hearts. These results indicate that NH 3 at physiological or low concentrations may play a modulatory role in heart function, but at high concentrations had a damaging effect on isolated rat hearts.

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Ammonia-induced taurine release from cultured rabbit m�ller cells is an osmoresistant process mediated by intracellular accumulation of cyclic AMP

Cited by 23 publications

References 23 publications

Taurine Interaction with Neurotransmitter Receptors in the CNS: An Update

Taurine Interaction with Neurotransmitter Receptors in the CNS: An Update

The Role of Protein Kinase C and Cyclic AMP in the Ammonia-Induced Shift of the Taurine Uptake/Efflux Balance Towards Efflux in C6 Cells

The inotropic effects of ammonia on isolated perfused rat hearts and the mechanisms involved

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