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Figure 3 | Molecular Pain

Figure 3

From: Homer1a signaling in the amygdala counteracts pain-related synaptic plasticity, mGluR1 function and pain behaviors

Figure 3

Synaptic transmission in the amygdala in brain slices from wild type and transgenic mice. Whole-cell patch recordings of excitatory transmission at the BLA-CeLC synapse in brain slices from wild-type and Homer1a overexpressing mice (H1a-mice) with and without arthritis (6 h postinduction). (A) Input-output functions of monosynaptic EPSCs in CeLC neurons increased in wild-type mice with arthritis (n = 5 neurons) compared to mice without arthritis (normal; n = 4) (B) Input-output functions of monosynaptic EPSCs in CeLC neurons were not different in brain slices from H1a-mice with arthritis (n = 5 neurons) and without arthritis (n = 4). (C) Monosynaptic EPSCs recorded in an individual CeLC neuron in a brain slice from an arthritic wild-type mouse and in another CeLC neuron from an arthritic H1a-mouse before and during CPCCOEt (10 μM; average of 8-10 traces). (D) CPCCOEt (10 μM) inhibited EPSCs in slices from arthritic wild-type mice (n = 5 neurons) but not in slices from arthritic H1a-mice (n = 5 neurons). Bar histograms show normalized drug effects (expressed as percent of predrug control, set to 100%). ** P < 0.01 (compared to predrug control in the same neurons; paired t-test).

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