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Taurine activates delayed rectifier Kv channels via a metabotropic pathway in retinal neurons
Simon Bulley1, Yufei Liu, Harris Ripps
1Department of Biomedical Science, Charles E Schmidt College of Medicine, Florida Atlantic University, Boca Raton, FL 33431, USA.
Abstract:
Taurine is one of the most abundant amino acids in the retina, throughout the CNS, and in heart and muscle cells. In keeping with its broad tissue distribution, taurine serves as a modulator of numerous basic processes, such as enzyme activity, cell development, myocardial function and cytoprotection. Despite this multitude of functional roles, the precise mechanism underlying taurine's actions has not yet been identified. In this study we report findings that indicate a novel role for taurine in the regulation of voltage-gated delayed rectifier potassium (K(V)) channels in retinal neurons by means of a metabotropic receptor pathway. The metabotropic taurine response was insensitive to the Cl(-) channel blockers, picrotoxin and strychnine, but it was inhibited by a specific serotonin 5-HT(2A) receptor antagonist, MDL11939. Moreover, we found that taurine enhanced K(V) channels via intracellular protein kinase C-mediated pathways. When 5-HT(2A) receptors were expressed in human embryonic kidney cells, taurine and AL34662, a non-specific 5-HT(2) receptor activator, produced a similar regulation of K(IR) channels. In sum, this study provides new evidence that taurine activates a serotonin system, apparently via 5-HT(2A) receptors and related intracellular pathways.
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