Figure 1From: Pain-related increase of excitatory transmission and decrease of inhibitory transmission in the central nucleus of the amygdala are mediated by mGluR1 Monosynaptic excitatory and polysynaptic inhibitory synaptic transmission in CeLC neurons. (A) Coronal brain slices containing the right amygdala were obtained from normal rats and arthritic rats 4-6 h after injections of kaolin and carrageenan (K/C) into the left knee joint. Magnified area shows position of the patch-clamp electrode ("Recording") in the CeLC; stimulation electrode in the BLA to activate direct glutamatergic projections and indirect disynaptic connections that involve GABAergic neurons in the intercalated cell masses (ITC). Diagrams are from [66]. (B) Biphasic synaptic responses were evoked at different holding potentials (-70, -30, and 0 mV). (C) Individual traces (average of 8-10) of synaptic responses evoked at -70 mV (downward deflections, EPSCs; inhibited by NBQX, 10 μM) and at 0 mV (upward deflections, IPSCs; blocked by bicuculline, 10 μM). Scale bars, 50 pA, 30 ms. (D) Monosynaptic EPSCs, but not polysynaptic IPSCs, follow high-frequency stimulation (20 Hz; 6 individual traces each). Scale bars, 50 pA, 30 ms. (E) Individual EPSCs and IPSCs evoked with twice-threshold stimulation (30 sweeps each). Latencies of IPSCs were longer and more variable. Calibration: 50 pA, 3 ms. (F) Distribution of EPSC and IPSC latencies measured from stimulus artifact to onset of synaptic current in one neuron (n = 100 events). (G) Bar histograms show average latencies (means ± SE) of EPSCs and IPSCs in 10 neurons. ** P < 0.01, paired t-test. (H) Bar histograms show the number of neurons that did not respond to the second or third high-frequency stimulus (HFS, 20 Hz). The failure rate is normalized for each neuron and averaged across the sample of neurons (n = 15; 0, no failure; 1, no IPSC). ** P < 0.01, compared to 1st stimulus (no failure), Dunnett's multiple comparison test.Back to article page