N-Ethylmaleimide Blocks Depolarization-Induced Suppression of Inhibition and Enhances GABA Release in the Rat Hippocampal Slice In Vitro

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Fig. 1.
Fig. 1.

NEM blocks iontophoretic baclofen responses. Whole-cell voltage-clamp recordings from a CA1 pyramidal cell in the presence of APV and CNQX (see Materials and Methods). Sharp upward deflections represent monosynaptic GABA IPSCs elicited at 10 sec intervals. The slow outward currents were elicited by iontophoretic ejection of baclofen at 3 min intervals shown byarrowheads (350 nA for 1 sec; iontophoretic pipette contained 40 mm baclofen). Responses in the top row were obtained in control solution. In control solution, baclofen also reduced the evoked IPSCs, probably via activation of presynaptic GABAB receptors. Lower traceswere obtained immediately after a 10 min application of 250 μm NEM. Note that NEM virtually abolished the postsynaptic baclofen response with very little effect on the baseline GABAA IPSC, but the IPSCs were no longer reduced by baclofen. The results suggest that NEM can block the G-protein-coupled responses mediated by both presynaptic and postsynaptic GABAB receptors. KCH3SO3-containing electrodes without QX-314 included were used in these experiments.VH = −60 mV.

  1. The Journal of Neuroscience vol. 17 no. 3 941-950
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