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- W4247805513 abstract "Application of 0.1–10 μM GABA in the vicinity of cultured embryonic rat thalamic neurons recorded with patch pipettes in the presence of 2 μM TTX induced or increased the frequency of miniature synaptic currents (MSCs) that reversed polarity at the Cl− equilibrium potential. These MSCs were blocked by the GABAA receptor antagonist bicuculline and exhibited exponential decay kinetics that closely paralleled those estimated from fluctuation analysis of Cl− channels activated pharmacologically by applying 1–10 μM GABA to the same cells. We conclude that the MSCs are mediated by GABA. Application of the GABAA receptor agonist muscimol activated Cl− current but failed to induce GABAergic MSCs while submicromolar concentrations of GABA evoked GABAergic MSCs but did not activate Cl− channels. The GABAB receptor agonist (-)baclofen did not mimic GABA in inducing MSCs. Induction of GABAergic MSCs by GABA required extracellular Ca2+. Verapamil and Co2+, which block voltage-dependent calcium channels, completely blocked GABA-induced MSCs independent of their effects on the direct activation of a Cl− current response. The results indicate that GABA can trigger GABAergic Cl−-dependent MSCs in a Cao2+-dependent manner. The mechanism may involve a novel receptor and/or signal transduction pathway. Synapse 25:15–23, 1997. © 1997 Wiley-Liss, Inc. 1 This article is a US Government work and, as such, is in the public domain in the United States of America." @default.
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- W4247805513 date "1997-01-01" @default.
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- W4247805513 title "GABA induces GABAergic MSCs in cultured embryonic rat thalamic neurons" @default.
- W4247805513 doi "https://doi.org/10.1002/(sici)1098-2396(199701)25:1<15::aid-syn2>3.3.co;2-r" @default.
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