EPAC1 and EPAC2 promote nociceptor hyperactivity associated with chronic pain after spinal cord injury.

2 B), with an apparent trend for rheobase to decrease ( Fig. 2 C).

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No significant differences were found between the incidence of large DSFs after SCI in neurons from wild-type mice and from EPAC2 −/− or EPAC1 −/− mice at RMP or when depolarized to −45 mV, although there was a possible trend for reduced incidence of large DSFs at RMP in the EPAC1 −/− mice ( Fig. 5 C).

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