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Since it was first reported approximately 40 years ago that putative amino acid neurotransmitters, including GABA, would likely be inactivated by synaptic high-affinity transporters, there has been an exponential increase in interest in delineating the pharmacological characteristics of these transporters. During the 1980s and 1990s a large series of publications was devoted to a detailed characterization of neuronal and astroglial GABA transporters demonstrating important differences between these, a notion that turned out to be of relevance for the development of anticonvulsants targeting GABA transporters. The cloning era, leading to the identification of four proteins capable of transporting GABA across plasma membranes, has further boosted this research. Ultimately the clinically active antiepileptic drug, tiagabine, was developed and it was established that its mechanism of action involved inhibition of the GABA transporter-I (GATI). Current and future research is directed towards a better understanding of how extrasynaptic GABA receptors may be regulated via manipulation of extrasynaptic GABA levels, possibly involving extrasynaptic GABA transporters, most likely non-GATI transporters.
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Reference:
Benzisoxazole – Wikipedia,
,Benzisoxazole – an overview | ScienceDirect Topics