• S J Hu, X J Song, K W Greenquist, J M Zhang, and R H LaMotte.
• Department of Anesthesiology, Yale University School of Medicine, 333 Cedar Street, New Haven, CT 06520-8051, USA.
• Pain. 2001 Oct 1; 94 (1): 39-46.

AbstractProtein kinase A (PKA) can play a critical role in the modulation of neuronal excitability. We examined the role of PKA in the modulation of abnormal spontaneous activity (SA) originating from the chronically compressed dorsal root ganglion (CCD). The L(4) and L(5) dorsal root ganglia (DRGs) were compressed by inserting a stainless steel rod into each corresponding intervertebral foramen. After 1-14 postoperative days, SA in DRG neurons with myelinated axons was recorded in vitro from teased dorsal root microfilaments. Rp-cAMPS (5-500 microM), a specific inhibitor of PKA, caused a dose-dependent decrease in the discharge rate of SA when topically applied to the DRG. The highest dose completely blocked the SA, but not the conduction of action potentials. H89 (10 microM), another PKA inhibitor, also markedly decreased SA. Sp-cAMPS (500 microM), a specific activator of PKA, increased the discharge rate of SA in all injured units tested, but did not trigger firing in silent neurons. Okadaic acid (0.1 microM), a protein phosphatase inhibitor, and forskolin (1 microM), an adenyl cyclase activator, each significantly increased the discharge rate of SA. These results strongly suggest that PKA modulates the SA in injured DRG neurons with myelinated axons.

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