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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
 
 
 
 

Pharmacological discrimination between gamma-aminobutyric acid type B receptors regulating cholecystokinin and somatostatin release from rat neocortex synaptosomes.

The gamma-aminobutyric acid (GABA)B receptors modulating the depolarization-evoked release of somatostatin (SRIF) or cholecystokinin ( CCK) from superfused rat cerebrocortical synaptosomes have been characterized pharmacologically. GABA inhibited the 15 mM KCl-evoked overflow of both SRIF and CCK; the EC50 values were 1.3 microM and 1.4 microM, respectively. The GABAB receptor agonist (-)-baclofen also diminished the release of SRIF (EC50 = 1.9 microM) and CCK (EC50 = 2.6 microM). The novel compound CGP 47656, a highly selective GABAB receptor ligand, inhibited the release of SRIF, with its affinity and efficacy being similar to those of GABA or (-)-baclofen; however, the compound was unable to affect CCK release even when tested at 300 microM. The GABAB receptor antagonist phaclofen prevented, with identical affinities, the effects of (-)-baclofen on SRIF (pKb = 4.9) and CCK (pKb = 4.8) release. The same was true for CGP 35348, another GABAB receptor antagonist, which blocked (-)-baclofen with a pKb value of 6.1 at both the GABAB receptors regulating SRIF and CCK release. The effects of (-)-baclofen were also counteracted by the novel GABAB receptor antagonist CGP 52432. However, the affinity of the drug at the GABAB receptors modulating SRIF release (pKb = 6.2) was about 30-fold lower than that at the receptors regulating CCK release (pKb = 7.6). The data suggest that the GABAB receptors situated on nerve terminals releasing SRIF and CCK display pharmacological heterogeneity and may represent different subtypes of GABAB receptors.[1]

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