CGP 52432: a novel potent and selective GABAB autoreceptor antagonist in rat cerebral cortex
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2024, Journal of Traditional and Complementary MedicineDisinhibition reduces extracellular glutamine and elevates extracellular glutamate in rat hippocampus in vivo
2015, Epilepsy ResearchCitation Excerpt :Other possible effects of GABABR blockade include (a) effect on presynaptic GABA autoreceptor, (b) antagonism of postsynaptic membrane hyperpolarization and the late inhibitory postsynaptic potential in pyramidal neurons (Olpe et al., 1990) and (c) elevation of cGMP mediated by the glutamate receptor/NO synthetase/guanylyl cyclase pathway (Fedele et al., 1997). In the present study, the effect on presynaptic GABA autoreceptor is likely to be small, because CGP 35348 is a weak blocker of GABA autoreceptor (Lanza et al., 1993). Also, elevation of cGMP is likely to be quite minor because CGP 35348 was delivered in aCSF containing normal (0.8 mM) Mg2+.
GABA <inf>B</inf> receptor-mediated selective peripheral analgesia by the non-proteinogenic amino acid, isovaline
2012, NeuroscienceCitation Excerpt :Whereas isovaline produced a locally restricted anti-allodynic effect at 5 μmol, we did not observe a locally restricted decrease in mechanical hypersensitivity at the doses tested for GABA or baclofen. The selective GABAB receptor antagonist, CGP52432 (Lanza et al., 1993), blocked the analgesic effects induced by near maximally effective doses of isovaline, GABA, or baclofen (Fig. 1B). Injected prior to PGE2 alone, CGP52432 did not increase PGE2-induced sensitivity.
GABA <inf>B</inf> receptors accentuate neural excitation contrast in rat insular cortex
2011, NeuroscienceCitation Excerpt :If these GABAB receptors were spontaneously activated, CGP 52432 should increase responsivity to the first stimulus by removing GABAB receptor-mediated suppression of glutamate release. In contrast, GABAB receptors may suppress spontaneous GABA release from inhibitory presynaptic terminals via autoreceptors (Lanza et al., 1993; Bailey et al., 2004; Takesian et al., 2010), as CGP 52432 sharpened the decay trajectory of responsivity to the first stimulus (Tseng and Haberly, 1988; McCormick, 1989; Fig. 4D). This explanation is supported by a report that rapid perfusion of a GABAB receptor antagonist increases the first inhibitory postsynaptic currents recorded from hippocampal cell pairs (Jensen et al., 1999).
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