Light deprivation slows but does not prevent the loss of photoreceptors in taurine transporter knockout mice.

UNLABELLED: Taurine transporter knockout mice show severe retinal degeneration at an early age. The study was designed to determine whether degeneration also takes place in the absence of light. Mice were maintained up to 6 weeks of age in cyclic lighting or in total darkness. Degeneration took place in both groups, but was more rapid in animals exposed to standard cyclic illumination. At the ultrastructural level the retinas showed features characteristic of apoptosis but not of necrosis. CONCLUSIONS: Cell differentiation is not seriously affected by the lack of a functional taurine transporter but mature photoreceptor cells do not survive without an intact transporter, even in the dark.

Taurine-induced long-lasting enhancement of synaptic transmission in mice: role of transporters.

Taurine, a major osmolyte in the brain evokes a long-lasting enhancement (LLETAU) of synaptic transmission in hippocampal and cortico-striatal slices. Hippocampal LLETAU was abolished by the GABA uptake blocker nipecotic acid (NPA) but not by the taurine-uptake inhibitor guanidinoethyl sulphonate (GES). Striatal LLETAU was sensitive to GES but not to NPA. Semiquantitative PCR analysis and immunohistochemistry revealed that taurine transporter expression is significantly higher in the striatum than in the hippocampus. Taurine transporter-deficient mice displayed very low taurine levels in both structures and a low ability to develop LLETAU in the striatum, but not in the hippocampus. The different mechanisms of taurine-induced synaptic plasticity may reflect the different vulnerabilities of these brain regions under pathological conditions that are accompanied by osmotic changes such as hepatic encephalopathy.