Activation of CB1 inhibits NGF-induced sensitization of TRPV1 in adult mouse afferent neurons

• Published in: Neuroscience 2014-09, Vol.277, p.679-689
• Main Authors: Wang, Z.-Y, McDowell, T, Wang, P, Alvarez, R, Gomez, T, Bjorling, D.E
• Format: Article
• Language: English
• Subjects: Animals; Arachidonic Acids - pharmacology; Calcium - metabolism; cannabinoid receptor 1; Cannabinoid Receptor Agonists - pharmacology; capsaicin; Capsaicin - pharmacology; Cells, Cultured; Enzyme Inhibitors - pharmacology; Ganglia, Spinal - drug effects; Ganglia, Spinal - physiology; Intracellular Space - drug effects; Intracellular Space - metabolism; Male; Mice, Inbred C57BL; nerve growth factor; Nerve Growth Factor - metabolism; Neurology; Neurons, Afferent - drug effects; Neurons, Afferent - physiology; Phosphatidylinositol 3-Kinases - antagonists & inhibitors; Phosphatidylinositol 3-Kinases - metabolism; Phosphorylation - drug effects; phosphorylation of AKT; Proto-Oncogene Proteins c-akt - metabolism; Receptor, Cannabinoid, CB1 - agonists; Receptor, Cannabinoid, CB1 - metabolism; Receptor, trkA - metabolism; sensitization; Sensory System Agents - pharmacology; transient receptor potential vanilloid 1; TRPV Cation Channels - metabolism
• ISSN: 0306-4522; 1873-7544
• DOI: 10.1016/j.neuroscience.2014.07.041

Highlights • CB1, trkA, and TRPV1 are co-localized in a subpopulation of adult mouse afferent neurons. • NGF increased the number of neurons that responded to capsaicin. • CB1 agonist ACEA (10 nM) inhibited the NGF-induced responses. • ACEA inhibited NGF-induced phosphorylation of AKT. • Blocking PI3 kinase activity attenuated the NGF-induced responses.