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• W1429721700 endingPage "263" @default.
• W1429721700 startingPage "215" @default.
• W1429721700 abstract "About 30% of neurons in the brain, particularly small interneurons, are thought to be gamma-aminobutyric acid (GABA)ergic (contain GAD) and most neurons responds to γ-Aminobutyric acid (GABA) by reducing their firing rate. The receptors mediating this effect are designated A and B. GABAA receptors, blocked by bicuculline, are found on virtually all neurons, both pre- and postsynaptically. Much of the interest in GABAA receptors arises from their being the major site of action of the benzodiazepines, a very important class of drugs used as anticonvulsants, sedative-hypnotics, muscle relaxants, and antianxiety agents. Not all chloride channel-linked GABA receptors are modulated by benzodiazepines; however, not all benzodiazepine effects are GABA related. The structural basis of these observations has become clearer with the cloning of many subunits of the GABAA receptor and the partial delineation of their functional roles. Recent cloning of subunits has changed the picture of receptor composition from four to five subunits. More refined protein chemistry has revealed the existence of multiple α- and β-subunit isoforms that have mostly been identified with specific complementary DNAs (cDNAs), using selective antibodies. This chapter emphasizes such recent findings." @default.
• W1429721700 created "2016-06-24" @default.
• W1429721700 creator A5061327791 @default.
• W1429721700 date "1994-01-01" @default.
• W1429721700 modified "2023-09-28" @default.
• W1429721700 title "Chapter 9 GABAA Receptor-Activated Chloride Channels" @default.
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