Fig. 1
Prenatal alcohol exposure (PAE) causes enhanced allodynia following standard sciatic damage and allodynic susceptibility following minor nerve damage. Hindpaw response thresholds from (a, b) minor (1-suture) vs (c, d) standard (4-suture) unilateral sciatic nerve injury (CCI) in middle-aged PAE rats. a–d All Sac and PAE rats displayed similar baseline hindpaw sensitivity responses following application of mechanical stimuli [ipsilateral, F2,30 = 1.877, p = 1.102; contralateral, F2,30 = 0.409, p = 0.668]. Following surgical sciatic nerve manipulation, a main effect of alcohol exposure [ipsilateral, F1,30 = 56.721, p < 0.0001; contralateral, F1,30 = 11.868, p = 0.002], surgery [ipsilateral, F2,30 = 155.795, p < 0.0001; contralateral, F2,30 = 99.261, p < 0.0001], and an interaction between alcohol exposure and surgery was seen [ipsilateral, F2,30 = 13.785, p < 0.0001; contralateral, F2,30 = 4.860, p = 0.015]. a, b Following minor CCI, PAE rats developed increased sensitivity whereas Sac rats did not. A main effect of alcohol exposure [ipsilateral, F1,30 = 61.875, p < .0001; contralateral, F1,30 = 12.857, p = 0.001], surgery [ipsilateral, F2,30 = 180.372, p < 0.0001; contralateral, F2,30 = 108.621, p < 0.0001], as well as an interaction between alcohol exposure and surgery was revealed [ipsilateral, F2,30 = 1.716, p < 0.0001; contralateral, F2,30 = 5.276, p = 0.011]. Asterisks indicate p < 0.05. The data are presented as the mean ± SEM