Changes in gene expression at inhibitory synapses in response to taurine treatment

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Abstract

We have previously shown that chronic supplementation of taurine to mice significantly ameliorated the age-dependent decline in memory acquisition and retention. We also showed that concomitant with the amelioration in cognitive function, taurine caused significant alterations in the GABAergic and somatonergic system. These changes include increased levels of the neurotransmitters GABA and glutamate, increased expression of both isoforms of GAD and the neuropeptide somatostatin, decreased hippocampal expression of the beta ( β ) 2/3 subunits of the GABA A receptor, an increase in the number of somatostatin-positive neurons, and an increase in the amplitude and duration of population spikes recorded from CA1 in response to Schaefer collateral stimulation and enhanced paired pulse facilitation in the hippocampus. These specific alterations of the inhibitory system caused by taurine treatment oppose those naturally induced by aging, suggesting a protective role of taurine in this process. In this study, we further investigated the effects of taurine on gene expression of relevant proteins of the inhibitory synapses using qRT-PCR method and found that taurine affects gene expression of various subunits of the GABA A receptors and GAD. Increased understanding the effects of taurine on gene expression will increase our understanding of age-related taurine-mediated neurochemical changes in the GABAergic system and will be important in elucidating the underpinnings of the functional changes of aging. Taurine might help forestall the age-related decline in cognitive functions through interaction with the GABAergic system. © Springer Science+Business Media New York 2013.

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Shen, C. H., Lempert, E., Butt, I., Neuwirth, L. S., Yan, X., & El Idrissi, A. (2013). Changes in gene expression at inhibitory synapses in response to taurine treatment. Advances in Experimental Medicine and Biology, 775, 187–194. https://doi.org/10.1007/978-1-4614-6130-2_16

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