Fig. 3. Quantification of gabapentin (GBP) concentration response and effect of AMPA antagonist on phosphorylated cyclic adenosine monophosphate response element binding protein (pCREB) activation in brainstem slices from normal and spinal nerve–ligated (SNL) rats. Data are presented as percentage of pCREB immunoreactivity (IR) in dopamine-β-hydroxylase–immunoreactive (DBH-IR) neurons. (  A ) Brainstem slices from normal (n = 4) and SNL (n = 4 or 5) rats were treated with vehicle and GBP (1–100 μm) for 30 min. *  P < 0.05  versus normal by two-way analysis of variance. #  P < 0.05  versus vehicle by one-way analysis of variance. (  B ) Brainstem slices from SNL rats were treated with vehicle (n = 5), GBP (100 μm, n = 5), CNQX (50 μm, n = 4), and GBP plus CNQX (n = 4) for 30 min. #  P < 0.05  versus vehicle. $  P < 0.05  versus GBP. 

Fig. 3. Quantification of gabapentin (GBP) concentration response and effect of AMPA antagonist on phosphorylated cyclic adenosine monophosphate response element binding protein (pCREB) activation in brainstem slices from normal and spinal nerve–ligated (SNL) rats. Data are presented as percentage of pCREB immunoreactivity (IR) in dopamine-β-hydroxylase–immunoreactive (DBH-IR) neurons. (  A ) Brainstem slices from normal (n = 4) and SNL (n = 4 or 5) rats were treated with vehicle and GBP (1–100 μm) for 30 min. *  P < 0.05  versus normal by two-way analysis of variance. #  P < 0.05  versus vehicle by one-way analysis of variance. (  B ) Brainstem slices from SNL rats were treated with vehicle (n = 5), GBP (100 μm, n = 5), CNQX (50 μm, n = 4), and GBP plus CNQX (n = 4) for 30 min. #  P < 0.05  versus vehicle. $  P < 0.05  versus GBP. 

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