Fig. 2: Ongoing pain does not alter MOR agonist synaptic effects or probability of glutamate release in the LHb.

Responses to the MOR agonist DAMGO were recorded in voltage clamp, V_m = −60 mV. a In animals with SNI, a subset of neurons responded to bath application of the MOR agonist DAMGO (500 nM) with a time locked outward current that was reversed with the MOR selective antagonist CTAP (500 nM). Line indicates mean, shading indicates SEM. n = 15 neurons from 4 rats. b Postsynaptic holding current changes in response to bath application of DAMGO were not different between neurons from naïve and SNI rats: Unpaired t-test df = 29, t = 0.87, p = 0.39. Filled circles indicate cells statistically determined to be “responsive” to DAMGO with within cell unpaired t tests. Gray bars indicate 25^th and 75^th percentiles. Naïve data: n = 17 neurons from 7 rats. c In rats with SNI, DAMGO (500 nM) induced a time-locked inhibition of electrically evoked glutamatergic EPSCs, and CTAP (500 nM) partially reversed the effect. Mean ± SEM. n = 15 neurons from 4 rats. d-This DAMGO inhibition of electrically evoked EPSC amplitude was not different between LHb neurons from naïve and SNI rats: Unpaired t-test df = 23, t = 0.47, p = 0.64. Naïve data: n = 10 neurons from 4 rats. Baseline probability of release at glutamatergic synapses was similar between LHb neurons in naïve and SNI rats as measured by (e) paired pulse ratio (P2/P1) of electrically stimulated EPSCs (50 ms interstimulus interval): Unpaired t-test, df = 24, t = 0.102, p = 0.92; (f) baseline spontaneous EPSC frequency: Unpaired t-test unequal variances, df = 37, t = −0.17, p = 0.87; and (g) spontaneous EPSC amplitude: Unpaired t-test unequal variances, df = 38, t = −0.09, p = 0.93. Data from naïve rats previously published in¹⁸. Tests are two-tailed.