Journal
JOURNAL OF NEURAL TRANSMISSION
Volume 107, Issue 10, Pages 1101-1116Publisher
SPRINGER-VERLAG WIEN
DOI: 10.1007/s007020070024
Keywords
GABA(B) receptor; G protein; N-ethylmaleimide (NEM); suramin; benzalkonium chloride; high-affinity GTPase activity
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Although it is known that GABA(B) receptors are negatively coupled to adenylyl cyclase, the detailed selectivity of functional interaction between GABA(B) receptors and G(i) subfamily members is still ambiguous. (+/-)-Baclofen-stimulated high-affinity GTPase activity, which was competitively antagonized by 2-hydroxy-saclofen, was attenuated by pretreatment of the membranes with N-ethylmaleimide (NEM) in a concentration- and incubation period-dependent manner. The NEM-pretreated (50 muM, 15 min at 4 degreesC) membranes restored the (+/-)-baclofen-sensitive high-affinity GTPase activity when reconstituted with pertussis toxin-sensitive bovine brain G proteins. Among recombinant rat G(alpha) subunits, G(i alpha -2) appeared most effective as compared with other subunits (G(i alpha -2) > G(i alpha -3) > G(i alpha -1) = G(o alpha)). The GABA(B) receptor-mediated high-affinity GTPase activity was also completely eliminated by 100 muM suramin and by 100 muM benzalkonium chloride. These results indicate that GABA(B) receptors in rat cerebral cortex couple to NEM-sensitive G proteins, in particular G(i2), which are sensitive to suramin and benzalkonium chloride.
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