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GABA<inf>B</inf> receptors: modulation of thalamocortical dynamics and synaptic plasticity
2021, NeuroscienceCitation Excerpt :Both isoforms are found in different locations; GABAB1a are mainly found in presynaptic terminals, where they control neurotransmitter release (Vigot et al., 2006), which depending on the specific type of synapse, excitatory or inhibitory, may inhibit or disinhibit respectively. The presynaptic action of GABAB-Rs inhibiting glutamate release occurs in many areas of the central nervous system (Willcockson et al., 1984; Dutar and Nicoll, 1988; Huston et al., 1995; Emri et al., 1996; Lin et al., 1996) and most probably in all cortical areas (Deisz and Prince, 1989; Kang, 1995; Ramoa and Sur, 1996; Ziakopoulos et al., 2000). GABAB-R-mediated inhibition requires the activation of the adenylyl cyclase/protein kinase A second messenger pathway, through the triggering of Gαi/o-type G proteins and liberation of Gβγ subunits, activating G protein-coupled inward-rectifying K+ channels and inhibition of voltage-gated Ca2+ channels (Bettler et al., 2004) (Figure 1).
Intracellular calcium chelation with BAPTA-AM modulates ethanol-induced behavioral effects in mice
2012, Experimental NeurologyBaclofen in cannabis dependence syndrome
2010, Biological PsychiatryGABA <inf>B</inf> receptor coupling to G-proteins and ion channels
2010, Advances in PharmacologyCitation Excerpt :The T-type CaV channels are low-voltage-activated, predominantly performing a pacemaker role; the other subtypes are high-voltage-activated. The GABAB receptor has been shown to couple specifically to the high-voltage-activated P-, Q-, and N- but not L- or R-type CaV channels (Guyon & Leresche, 1995; Harayama et al., 1998; Huston et al., 1995; Li & Stern, 2004; Mintz & Bean, 1993; Vigot et al., 2006). The electrophysiological relationship of GABAB-CaV has been extensively studied throughout the brain including the hippocampus (Doze et al., 1995; Wu & Saggau, 1995), SON (Li & Stern, 2004), DRG (Menon-Johansson et al., 1993), and midbrain (Cardozo & Bean, 1995).
Ischaemia differentially regulates GABA<inf>B</inf> receptor subunits in organotypic hippocampal slice cultures
2009, NeuropharmacologyCitation Excerpt :For example, activation of presynaptic GABAB receptors that can down-regulate glutamate release might provide a mechanism to counteract excitotoxic neuronal cell death. The GABAB receptor agonist baclofen inhibits glutamate release (Huston et al., 1995) and has been reported to be neuroprotective in vivo (Babcock et al., 2002; Jackson-Friedman et al., 1997; Lal et al., 1995; Ouyang et al., 2007) and in organotypic hippocampal slice cultures during oxygen–glucose deprivation (OGD) (Dave et al., 2005). It has also been reported that both GABAA and GABAB receptor agonists can protect neurons against death induced by ischaemia/reperfusion in vivo via a mechanism involving inhibition of NMDA receptor-mediated nitric oxide (NO) production by neuronal NO synthase (nNOS) (Zhou et al., 2008).