GABAB receptors and norepinephrine-stimulated cAMP production in rat brain cortex
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Cited by (69)
Bidirectional enantioselective effects of the GABA<inf>B</inf> receptor agonist baclofen in two mouse models of excessive ethanol consumption
2015, AlcoholCitation Excerpt :There may also be differences with how these molecules interact with other neurotransmitters. The (−)-baclofen isomer interacts with norepinephrine whereas R-baclofen may be responsible for other non-GABAergic effects of baclofen (Karbon, Duman, & Enna, 1984; Waddington & Cross, 1980). Individual differences in populations of GABAB receptors may increase or decrease the efficacy of racemic baclofen in reducing ethanol intake in preclinical models and in treating AUDs clinically.
Intra-nucleus accumbens shell injections of R(+)- and S(-)-baclofen bidirectionally alter binge-like ethanol, but not saccharin, intake in C57Bl/6J mice
2014, Behavioural Brain ResearchCitation Excerpt :Binding of baclofen relies not only on the absolute configuration of the drug (d/l or S/R), but also on the rotation of the molecule (+ or -). Both R- and S-baclofen are equally efficacious in displacing GABA from high and low affinity binding sites, but (−)baclofen is much more efficacious than (+)baclofen at displacing racemic baclofen at low affinity sites, which appear to be selective for (-)baclofen [53–55]. Further, these enantiomers interact differently with other neurotransmitters.
A legacy of discovery: From monoamines to GABA
2011, NeuropharmacologyCitation Excerpt :His studies in this area were aimed at defining the GABAB effector system and at characterizing a possible relationship between this receptor and the mechanism of action of antidepressants (Szekely et al., 1987; Wojcik et al., 1990; De Erausquin et al., 1992). This work influenced our studies in this area, both at the time and in subsequent years (Karbon et al., 1984; Karbon and Enna, 1985; Enna et al., 1986; Sands et al., 2004; Ghose et al., in press). Performing GABAA receptor solubilization experiments, Costa and co-workers demonstrated that the GABA and benzodiazepine recognitions sites reside on two different proteins (Massotti et al., 1981b; Mazzari et al., 1981).
Historical perspective and emergence of the GABA <inf>B</inf> receptor
2010, Advances in PharmacologyCitation Excerpt :A third signaling system associated with GABAB sites is adenylyl cyclase which is normally inhibited by receptor activation (Xu & Woczik, 1986). However, if the enzyme has been activated by Gs-coupled receptor agonists such as isoprenaline, the β-adrenoceptor ligand, GABAB receptor activation enhances the formation of cyclic adenosine monophosphate (cAMP) above the level achieved with isoprenaline alone (Hill, 1985; Karbon et al., 1984). This observation prompted a search for receptor subtypes by comparing the abilities of different GABAB receptor agonists to inhibit or enhance cAMP production.