TRPV1 is part of the transient receptor potential family and is one of the non-GPCR cannabinoid receptors. TRPV1 is involved in thermoregulation and pain detection (nociception).

Chemical Name: 
Transient receptor potential cation channel subfamily V member 1/Vanilloid receptor 1.
IUPHAR entry: 
Wikipedia entry: 
Distribution: 

TRPV1 is found in dorsal root ganglia, brain, kidney, pancreas, testes, uterus, spleen, stomach, small intestine, lung and liver.

Endocannabinoids: 
Literature Discussion: 

Endocannabinoids

Anandamide anti cancer properties depend on TRPV1 and not on CB1 or CB2 (Contassot et al., 2004; Ramer and Hinz, 2008).

cancer

Bone Cancer

Research shows that bone cancer cells express TRPV1 receptor  (Kawamata et al., 2010). 

Cervical Cancer

cannabinoid receptors CB1CB2 and TRPV1 are expressed in the cervix (Ayakannu et al., 2015).

Glioblastoma

CBD modulates Id-1 gene and targets receptors CB1, CB2, TRPV-1 and TRPV-2 (Solinas et al., 2013; Soroceanu et al., 2013)

Bulimia

OEA reduced food intake and weight gain in rodents via PPARα and TRPV1 (Overton et al., 2006).

Functional Gastro-intestinal disorders

Apart from CB1 and CB2, there is evidence for the involvement of PPARγ and TRPV1 in Crohn’s Disease (de Fontgalland et al., 2014; Schicho and Storr, 2014)

CB1 and TRPV1 signaling are both required for the development of stress-induced visceral hyperalgesia and TRPV4 and TRPA1 may also be involved (Lin et al., 2013).

Cystitis

In a rat study, Anandamide was found to induce bladder inflammation pain through TRPV1 suggesting this receptor might be a therapeutic target (Dinis et al., 2004).

Eczema

In an experimental mouse model of Eczema endocannabinoids AEA and PEA were increased and TRPV1 and PPARα were upregulated (Petrosino et al., 2010). PEA enhances AEA activity at CB1CB2 and TRPV1 receptors and protects against keratinocyte inflammation in a TRPV1-, but not CB1CB2 or PPARα-dependent way.

Epilepsy

In mice, stimulating CB1 receptors (ACEA) or blocking TRPV1 receptors (capsazepine) protected against PTZ-induced seizures (Naderi et al., 2015). Interestingly, co-administration of both compounds attenuated the anti-convulsive effect, suggesting an interaction between CB1 and TRPV1 mediated signaling.

References:

Ayakannu, T., Taylor, A.H., Willets, J.M., and Konje, J.C. (2015). The evolving role of the endocannabinoid system in gynaecological cancer. Hum. Reprod. Update 21, 517–535.

Contassot, E., Tenan, M., Schnüriger, V., Pelte, M.-F., and Dietrich, P.-Y. (2004). Arachidonyl ethanolamide induces apoptosis of uterine cervix cancer cells via aberrantly expressed vanilloid receptor-1. Gynecol. Oncol. 93, 182–188.

De Fontgalland, D., Brookes, S.J., Gibbins, I., Sia, T.C., and Wattchow, D.A. (2014). The neurochemical changes in the innervation of human colonic mesenteric and submucosal blood vessels in ulcerative colitis and Crohn’s disease. Neurogastroenterol. Motil. Off. J. Eur. Gastrointest. Motil. Soc. 26, 731–744.

Dinis, P., Charrua, A., Avelino, A., Yaqoob, M., Bevan, S., Nagy, I., and Cruz, F. (2004). Anandamide-evoked activation of vanilloid receptor 1 contributes to the development of bladder hyperreflexia and nociceptive transmission to spinal dorsal horn neurons in Cystitis. J. Neurosci. Off. J. Soc. Neurosci. 24, 11253–11263.

Kawamata, T., Niiyama, Y., Yamamoto, J., and Furuse, S. (2010).Reduction of bone cancer pain by CB1 activation and TRPV1 inhibition. J. Anesth. 24, 328–332.

Lin, X.-H., Wang, Y.-Q., Wang, H.-C., Ren, X.-Q., and Li, Y.-Y. (2013). Role of endogenous cannabinoid system in the gut. Sheng Li Xue Bao 65, 451–460.

Naderi, N., Shafieirad, E., Lakpoor, D., Rahimi, A., and Mousavi, Z. (2015). Interaction between cannabinoid Compounds and Capsazepine in Protection against Acute Pentylenetetrazole-induced Seizure in Mice. Iran. J. Pharm. Res. IJPR 14, 115–120.

Overton, H.A., Babbs, A.J., Doel, S.M., Fyfe, M.C.T., Gardner, L.S., Griffin, G., Jackson, H.C., Procter, M.J., Rasamison, C.M., Tang-Christensen, M., et al. (2006). Deorphanization of a G protein-coupled receptor for oleoylethanolamide and its use in the discovery of small-molecule hypophagic agents. Cell Metab. 3, 167–175.

Petrosino, S., Cristino, L., Karsak, M., Gaffal, E., Ueda, N., Tüting, T., Bisogno, T., De Filippis, D., D’Amico, A., Saturnino, C., et al. (2010). Protective role of palmitoylethanolamide in contact allergic dermatitis. Allergy 65, 698–711.

Ramer, R., and Hinz, B. (2008). Inhibition of cancer cell invasion by cannabinoids via increased expression of tissue inhibitor of matrix metalloproteinases-1. J. Natl. cancer Inst. 100, 59–69.

Schicho, R., and Storr, M. (2014). Cannabis finds its way into treatment of Crohn’s disease. Pharmacology 93, 1–3.

Solinas, M., Massi, P., Cinquina, V., Valenti, M., Bolognini, D., Gariboldi, M., Monti, E., Rubino, T., and Parolaro, D. (2013). Cannabidiol, a Non-Psychoactive cannabinoid Compound, Inhibits Proliferation and Invasion in U87-MG and T98G Glioma Cells through a Multitarget Effect. PLoS ONE 8.

Soroceanu, L., Murase, R., Limbad, C., Singer, E., Allison, J., Adrados, I., Kawamura, R., Pakdel, A., Fukuyo, Y., Nguyen, D., et al. (2013). Id-1 is a key transcriptional regulator of glioblastoma aggressiveness and a novel therapeutic target. cancer Res. 73, 1559–1569.