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The GABAC receptor is also linked to chloride channels, with distinct physiological and pharmacological properties. In contrast to the fast and transient responses elicited from GABAA receptors, GABAC receptors mediate slow and sustained responses. Pharmacologically, GABAC receptors are bicuculline- and baclofen-insensitive, and are not modulated by many GABAA receptor modulators (such as benzodiazepines and barbiturates and neuroactive steroids). The GABAC receptors are activated by cis-aminocrotonic acid (CACA), which is not recognised by either the GABAA or GABAB receptors, suggesting that they recognise the partially folded conformation of GABA. GABAC receptors, like GABAA receptors are blocked by picrotoxin, while 1,2,5,6-tetrahydropyridine-4-yl methyl phosphinic acid (TPMPA) appears to inhibit GABAC receptors selectively. However, molecular cloning studies have revealed that this pharmacological profile is remarkably similar. Like other ligand-gated ion channels, the molecule is probably formed by five subunits arranged around a central pore. Like the GABAA channel, the pore, when open, is permeable to chloride ions, though its conductance is smaller than that of GABAA. The genes for GABAC are encoded on chromosome 6 in humans, distinct from the clusters of GABAA receptor subunit genes which are found on chromosomes 4, 5, 15 and X.