Neuroprotective effect of taurine against focal cerebral ischemia in rats possibly mediated by activation of both GABAA and glycine receptors

Preservation of GABA A Receptor Function by PTEN Inhibition Protects Against Neuronal Death in Ischemic Stroke

“…28,29 However, an ischemic insult profoundly shifts the balance in the direction of overexcitation due to the excess release of excitatory amino acids and/or suppression of the GABA-ergic system. [5][6][7][8][9] The present study provides evidence supporting the notion that GABA A R function is suppressed in OGD-treated neurons and that the reduced GABA A R expression may contribute to OGD insult-induced suppression of GABA A R function. [5][6][7][8][9]11 Thus, preserving or enhancing GABA A R function and expression may be a potential strategy to protect against ischemic neuron death.…”

“…Although enhancing GABA A R function by GABA A R agonists has been shown to protect against delayed neuronal death in experimental models of cerebral ischemia, 5,10,30,31 use of GABA A R agonists as neuroprotective agents has been disappointing in clinical trials. 5,12,[32][33][34] One simple explanation is that the adverse effects may be caused by agonistinduced global overactivation of GABA A Rs, which would not only lead to an antiexcitotoxicity effect but also result in unwanted activities mediated by GABA A R overactivation.…”

“…5,12,[32][33][34] One simple explanation is that the adverse effects may be caused by agonistinduced global overactivation of GABA A Rs, which would not only lead to an antiexcitotoxicity effect but also result in unwanted activities mediated by GABA A R overactivation. The present results suggest that investigating intracellular signaling such as PTEN linked to GABA A Rs in ischemic neurons is a critical approach in future research.…”

“…Suppressed function of ␥-aminobutyric acid subtype A receptors (GABA A Rs) causes neuronal damage after stroke. [5][6][7][8] Both the GABA uptake inhibitor and the GABA A R agonist are neuroprotective in animal models of ischemic stroke. 9,10 A recent study has shown that cell surface GABA A Rs are markedly decreased in neurons treated by oxygen-glucose deprivation (OGD), 11 suggesting that a change in the number of membrane GABA A Rs may be a crucial process in enhancing ischemic neuron death.…”

Sanjoinine A Isolated from Zizyphi Spinosi Semen Augments Pentobarbital-Induced Sleeping Behaviors through the Modification of GABA-ergic Systems

“…Because the activation of glycine receptors also increase chloride ion channels open that facilitate inhibitory neurotransmission in the mammalian in brain, it is also possible that sanjoinine A might increase Cl Ϫ influx by glycine receptors. 30,31) We tried to find out the typical responding subunits of the effective dosage of sanjoinine A, which might have at least a close relationship with the acting site by which sanjoinine A acts on GABA A receptors and exerts its sleeping potentiating effects. We also investigated the effects of sanjoinine A and pentobarbital on expression of GAD65/67 expression by western blot technique.…”