Abstract
It has been well documented that the binding of γ-aminobutyric acid (GABA), which is considered as an inhibitory neurotransmitter in the mammalian central nervous system (CNS), to its relevant receptor at GABAergic synapses induces the increased influx of chloride ion and generates inhibitory postsynaptic potential (1,2). Recent neurochemical studies using 36C1− also have indicated that GABA induces the influx of 36C1− across synaptic membrane (3,4). Although these evidences suggest the presence of functional coupling between GABA receptor and chloride ion channel, it has been also proposed that there is an interaction between GABA agonists and benzodiazepines at GABAergic synapses (5,6). In fact, various pharmacological studies have shown that GABA and GABA agonists such as muscimol facilitate the benzodiazepine binding to benzodiazepine receptor (7,8,9,10), which is known as a pharmacologically relevant receptor for benzodiazepines (11,12,13), whereas benzodiazepines stimulate GABA receptor binding (9,10,14,15). Furthermore, biochemical studies have indicated that both GABA and benzodiazepine receptors are cosolubilized from cerebral synaptic membrane fraction by various detergents, and both binding sites appear in the same fraction following various column chromatographies (10,16,17,18). These results strongly suggest that cerebral GABA receptor may be functionally as well as structurally coupled with benzodiazepine receptor and chloride ion channel. In fact, we have reported that the purification of cerebral GABA receptor coupled with benzodiazepine receptor is achieved by the use of benzodiazepine affinity column (19).
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Kuriyama, K., Taguchi, Ji. (1988). Biochemical and Functional Properties of Purified GABA Receptor/Benzodiazepine Receptor/Chloride Channel Complex and Application of its Antibody for Immunohistochemical Studies. In: Kito, S., Segawa, T., Kuriyama, K., Tohyama, M., Olsen, R.W. (eds) Neuroreceptors and Signal Transduction. Advances in Experimental Medicine and Biology, vol 236. Springer, Boston, MA. https://doi.org/10.1007/978-1-4757-5971-6_2
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