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. 2001 Jan 1;21(1):59–66. doi: 10.1523/JNEUROSCI.21-01-00059.2001

Fig. 5.

Fig. 5.

Kainate receptor activation suppresses primary afferent neurotransmission in spinal cord slices. A, A diagram illustrates the placement of stimulating and recording electrodes in the dorsal horn of a spinal slice. B, NMDA receptor-mediated EPSCs were isolated at a holding potential of +40 mV in the presence of 100 μm SYM2206. Traces from a representative neuron show reversible inhibition of EPSCs by 0.1 μm KA. C, When 20 μm CNQX replaced SYM2206 in experiments, as in B, 0.1 μm KA had less of an effect. D, Kainate exerted a dose-dependent inhibition of NMDA receptor-mediated EPSCs (n = 3–4 cells per concentration).E, Summarized data showing inhibition of NMDA receptor-mediated EPSCs by 0.1 μm KA in the presence of 100 μm SYM2206 (KA; n= 3) that was sensitive to 20 μm CNQX (KA+ CNQX; n = 3). Treatment with 100 μm CNQX (n = 3) afforded no additional blockade of the effect of kainate (data not shown). In addition, AMPA receptor-mediated EPSCs were suppressed by application of 2 μm ATPA (n = 5). ATPA- and KA-induced EPSC suppression were both statistically significant (p < 0.05; paired t test comparing absolute EPSC amplitudes in control and test conditions). *p < 0.05 indicates a significant difference in EPSC reduction by KA in the presence of SYM2206 versus CNQX;t test comparing the percentage of EPSC suppression in each condition.