Endocannabinoid-Goα signalling inhibits axon regeneration in Caenorhabditis elegans by antagonizing Gqα-PKC-JNK signalling

Strahil Iv. Pastuhov, Kota Fujiki, Paola Nix, Shuka Kanao, Michael Bastiani, Kunihiro Matsumoto () and Naoki Hisamoto
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Strahil Iv. Pastuhov: Graduate school of Science, Nagoya University
Kota Fujiki: Graduate school of Science, Nagoya University
Paola Nix: University of Utah
Shuka Kanao: Graduate school of Science, Nagoya University
Michael Bastiani: University of Utah
Kunihiro Matsumoto: Graduate school of Science, Nagoya University
Naoki Hisamoto: Graduate school of Science, Nagoya University

Nature Communications, 2012, vol. 3, issue 1, 1-9

Abstract: Abstract The ability of neurons to regenerate their axons after injury is determined by a balance between cellular pathways that promote and those that inhibit regeneration. In Caenorhabditis elegans, axon regeneration is positively regulated by the c-Jun N-terminal kinase mitogen activated protein kinase pathway, which is activated by growth factor-receptor tyrosine kinase signalling. Here we show that fatty acid amide hydrolase-1, an enzyme involved in the degradation of the endocannabinoid anandamide (arachidonoyl ethanolamide), regulates the axon regeneration response of γ-aminobutyric acid neurons after laser axotomy. Exogenous arachidonoyl ethanolamide inhibits axon regeneration via the Goα subunit GOA-1, which antagonizes the Gqα subunit EGL-30. We further demonstrate that protein kinase C functions downstream of Gqα and activates the MLK-1-MEK-1-KGB-1 c-Jun N-terminal kinase pathway by phosphorylating MLK-1. Our results show that arachidonoyl ethanolamide induction of a G protein signal transduction pathway has a role in the inhibition of post-development axon regeneration.

Date: 2012
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DOI: 10.1038/ncomms2136

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