Rolipram reduces SCI-induced increases in PDE4B1 and PDE4A5 protein production as well as PDE4A5 phosphorylation.

<p><b>A–C.</b> Immunoblot analysis of injured spinal cord homogenates revealed an SCI-induced increase in PDE4B1 at 25 h that was significantly abrogated by Rolipram treatment, when given at either 1 or 24 h after SCI (<b>A, B</b>). PDE4D1/2 was not regulated by either SCI or Rolipram treatment at the protein level (<b>A, C</b>). <b>D–H.</b> Unlike PDE4A1 (<b>D–E</b>), PDE4A5 protein production (<b>F, G</b>) and phosphorylation (<b>F, H</b>) was increased from 4 to 25 h after SCI. Rolipram, when given at either 1 or 24 h after SCI (black and diagonal line bars, respectively), significantly abated these SCI-induced increases. Vehicle delivery (at 1 h, dotted white bars) did not affect the protein production or phosphorylation of the PDE4s examined post-SCI. Density readings of PDE4 bands were normalized to β-actin immunoreactivity performed on the same blots. Statistical significance indicated at *p<0.05, **p<0.01 or ***p<0.001 compared to injury only controls (white bars) and ^#p<0.05 or ^##p<0.01 compared to uninjured controls (gray bars). Error bars are expressed as SEMs.