American Society of Anesthesiologists

Fig. 2.

$The reduced γ-aminobutyric acidergic inhibition caused 61-kD isoform of striatal-enriched protein phosphatase (STEP61) dissociation with Fyn and extracellular signal–regulated kinase 1/2 (ERK1/2) in spinal dorsal horn of mice. (A) Intrathecal application of γ-aminobutyric acid type A receptor antagonist bicuculline (BIC; 0.1 μg) for 40 min did not affect STEP61 content at spinal homogenates (n = 6 experiments). The equal protein loadings were indicated by β-actin signals. (B) Bicuculline reduced the amounts of ERK1/2 and Fyn coimmunoprecipitated (Co-IP) by anti-STEP antibody from crude synaptosomal fraction, which was reversed by intrathecal application of cyclic adenosine 3’,5’-monophosphate–dependent protein kinase inhibitor H-89 (2.5 μg) for 30 min. Bicuculline had no effect on STEP61 interaction with p38 mitogen-activated protein kinase (p38). Non-specific immunoglobulin G (IgG) was used as control. The graph showed the percentage changes of protein contents precipitated by anti-STEP antibody. *P < 0.05 relative to saline control. #P < 0.05 relative to bicuculline-injected mice (n = 4 experiments). (C) Intrathecal application of H-89 alone did not affect STEP61 interaction with ERK1/2 and Fyn in intact mice (n = 4 experiments). IB = immunoblotted.$

The reduced γ-aminobutyric acidergic inhibition caused 61-kD isoform of striatal-enriched protein phosphatase (STEP61) dissociation with Fyn and extracellular signal–regulated kinase 1/2 (ERK1/2) in spinal dorsal horn of mice. (A) Intrathecal application of γ-aminobutyric acid type A receptor antagonist bicuculline (BIC; 0.1 μg) for 40 min did not affect STEP61 content at spinal homogenates (n = 6 experiments). The equal protein loadings were indicated by β-actin signals. (B) Bicuculline reduced the amounts of ERK1/2 and Fyn coimmunoprecipitated (Co-IP) by anti-STEP antibody from crude synaptosomal fraction, which was reversed by intrathecal application of cyclic adenosine 3’,5’-monophosphate–dependent protein kinase inhibitor H-89 (2.5 μg) for 30 min. Bicuculline had no effect on STEP61 interaction with p38 mitogen-activated protein kinase (p38). Non-specific immunoglobulin G (IgG) was used as control. The graph showed the percentage changes of protein contents precipitated by anti-STEP antibody. *P < 0.05 relative to saline control. #P < 0.05 relative to bicuculline-injected mice (n = 4 experiments). (C) Intrathecal application of H-89 alone did not affect STEP61 interaction with ERK1/2 and Fyn in intact mice (n = 4 experiments). IB = immunoblotted.

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