GABA induces GABAergic MSCs in cultured embryonic rat thalamic neurons

✍ Scribed by Qi-Ying Liu; Jean Vautrin; Anne E. Schaffner; Wu Ma; Jeffery L. Barker

• Publisher: John Wiley and Sons
• Year: 1997
• Tongue: English
• Weight: 158 KB
• Volume: 25
• Category: Article
• ISSN: 0887-4476
• DOI: 10.1002/(sici)1098-2396(199701)25:1<15::aid-syn2>3.0.co;2-i

✦ Synopsis

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 2 equilibrium potential. These MSCs were blocked by the GABA A receptor antagonist bicuculline and exhibited exponential decay kinetics that closely paralleled those estimated from fluctuation analysis of Cl 2 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 GABA A receptor agonist muscimol activated Cl 2 current but failed to induce GABAergic MSCs while submicromolar concentrations of GABA evoked GABAergic MSCs but did not activate Cl 2 channels. The GABA B receptor agonist (2)baclofen did not mimic GABA in inducing MSCs. Induction of GABAergic MSCs by GABA required extracellular Ca 21 . Verapamil and Co 21 , which block voltage-dependent calcium channels, completely blocked GABA-induced MSCs independent of their effects on the direct activation of a Cl 2 current response. The results indicate that GABA can trigger GABAergic Cl 2 -dependent MSCs in a Ca o 21 -dependent manner. The mechanism may involve a novel receptor and/or signal transduction pathway.