PI3Kγ integrates cAMP and Akt signalling of the μ-opioid receptor.

ABSTRACT:

Background and purpose

The μ-opioid receptor has been characterized as the main mediator of opioid signalling in neuronal cells. Opioid-induced pain suppression was originally proposed to be mediated by μ-opioid receptor-induced inhibitory effects on cAMP, which is known to mediate inflammatory hypernociception. Recent investigations revealed PI3Kγ and Akt (PKB) as additional elements of μ-opioid receptor signalling. Hence, we investigated the interaction between pronociceptive cAMP and antinociceptive PI3K/Akt signalling pathways.

Experimental approach

The human neuroblastoma cell line SK-N-LO and primary dorsal root ganglia (DRG) cells from mice were used to elucidate mediators of μ-opioid receptor signalling. In both cellular systems cAMP was manipulated by stimulation of

SUBMITTER: Madishetti S 

PROVIDER: S-EPMC4080984 | biostudies-literature | 2014 Jul

REPOSITORIES: biostudies-literature