γ-Aminobutyric acid-induced depression of calcium currents of chick sensory neurons
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The role of CA3 GABA<inf>B</inf> receptors on anxiolytic-like behaviors and avoidance memory deficit induced by D-AP5 with respect to Ca<sup>2 +</sup> ions
2017, Progress in Neuro-Psychopharmacology and Biological PsychiatryCitation Excerpt :GABA activates both ionotropic GABAA receptors (GABAARs) and metabotropic GABABRs. The activation of GABABRs, mediated through inhibitory G-proteins, induces K+-dependent hyperpolarization or slow IPSPs and inhibits voltage-gated calcium currents, which in turn change the transmitter release in both glutamatergic and GABAergic synapses (Chalifoux and Carter, 2011; Deisz and Lux, 1985; Gahwiler and Brown, 1985). GABAB autoreceptors are involved in prolongation of EPSPs and creating conditions required for the activation of the NMDAR currents that trigger LTP (Larson and Lynch, 1986).
GABA <inf>B</inf> receptor coupling to G-proteins and ion channels
2010, Advances in PharmacologyCitation Excerpt :Agonist activation of GABAB receptors stimulates Gi/o proteins (Menon-Johansson et al., 1993; Obrietan & van den Pol, 1999) releasing Gβγ to bind to, and inhibit, the high voltage-activated CaV channel (Dolphin, 2003) by 10–50 % (Guyon & Leresche, 1995; Huston et al., 1990; Menon-Johansson et al., 1993). This current inhibition is voltage-independent (Deisz & Lux, 1985) and is driven by a slowing of the CaV channel activation kinetics; as a result calcium influx is reduced, thereby decreasing various calcium-dependent, excitatory neuronal activities. For example, presynaptically, GABAB receptor-dependent inhibition of CaV currents leads to reduced neurotransmitter release.
GABA(B) receptor-mediated effects in human and rat neocortical neurones in vitro
1999, Neuropharmacology