(S)Pot on Mitochondria: Cannabinoids Disrupt Cellular Respiration to Limit Neuronal Activity

Tibor Harkany; Tamas L Horvath

doi:10.1016/j.cmet.2016.12.020

(S)Pot on Mitochondria: Cannabinoids Disrupt Cellular Respiration to Limit Neuronal Activity

Cell Metab. 2017 Jan 10;25(1):8-10. doi: 10.1016/j.cmet.2016.12.020.

Authors

Tibor Harkany¹, Tamas L Horvath²

Affiliations

¹ Department of Molecular Neurosciences, Center for Brain Research, Medical University of Vienna, 1090 Vienna, Austria; Department of Neuroscience, Karolinska Institutet, 17177 Stockholm, Sweden. Electronic address: tibor.harkany@meduniwien.ac.at.
² Program in Integrative Cell Signaling and Neurobiology of Metabolism, Section of Comparative Medicine, Yale University School of Medicine, New Haven, CT 06510, USA.

PMID: 28076767
DOI: 10.1016/j.cmet.2016.12.020

Abstract

Classical views posit G protein-coupled cannabinoid receptor 1s (CB1Rs) at the cell surface with cytosolic Giα-mediated signal transduction. Hebert-Chatelain et al. (2016) instead place CB₁Rs at mitochondria limiting neuronal respiration by soluble adenylyl cyclase-dependent modulation of complex I activity. Thus, neuronal bioenergetics link to synaptic plasticity and, globally, learning and memory.

Keywords: GPCR; THC; axonal growth; bioenergetics; cannabinoid; cannabinoid receptor 1; cannabis; endocannabinoid; mitochondrial import; respiration.

Publication types

Comment

MeSH terms

Cannabinoids*
Humans
Memory
Mitochondria*
Receptor, Cannabinoid, CB1
Receptors, Cannabinoid
Signal Transduction

Substances

Cannabinoids
Receptor, Cannabinoid, CB1
Receptors, Cannabinoid