Perspectives of TRPV1 Function on the Neurogenesis and Neural Plasticity

Abstract

The development of new strategies to renew and repair neuronal networks using neural plasticity induced by stem cell graft could enable new therapies to cure diseases that were considered lethal until now. In adequate microenvironment a neuronal progenitor must receive molecular signal of a specific cellular context to determine fate, differentiation, and location. TRPV1, a nonselective calcium channel, is expressed in neurogenic regions of the brain like the subgranular zone of the hippocampal dentate gyrus and the telencephalic subventricular zone, being valuable for neural differentiation and neural plasticity. Current data show that TRPV1 is involved in several neuronal functions as cytoskeleton dynamics, cell migration, survival, and regeneration of injured neurons, incorporating several stimuli in neurogenesis and network integration. The function of TRPV1 in the brain is under intensive investigation, due to multiple places where it has been detected and its sensitivity for different chemical and physical agonists, and a new role of TRPV1 in brain function is now emerging as a molecular tool for survival and control of neural stem cells.

TRPV1 Is Associated with Testicular Apoptosis in Mice

“…TRPV1 KO male mice lived 12% longer than their WT counterparts. The lifespan and longevity of TRPV1 KO mice examined in our study were similar to the findings of Riera et al (2014) (Barnes et al, 1998;De Toni et al, 2016), and TRPV1 activation induces apoptosis of many types of cells (Ramirez-Barrantes et al, 2016;Hou et al, 2019). Our study focused on testicular aging of TRPV1 KO mice by investigating cytological and histological changes.…”

Antiviral Effects of Menthol on Coxsackievirus B

“…We have found that members of the transient receptor potential (TRP) channels may be important for alterations in mitochondrial dynamics following CVB infection. TRPV1, commonly known as the heat and capsaicin-activated ion channel, has been shown to depolarize mitochondria and trigger mitochondrial fission following activation [23][24][25]. Our preliminary findings suggest that CVB relies on TRPV1-mediated mitochondrial fragmentation, and treating cells with the specific TRPV1 inhibitor, SB-366791, potently reduces CVB infection.…”

“…In an earlier report we had demonstrated that CVB infection induces mitochondrial fission, and inhibiting fission significantly impaired infection [19]. Connections between mitochondrial fission and the heat and capsaicin receptor TRPV1 had been documented previously [23][24][25], thus we sought to determine if temperature could influence CVB infection. To test this, we first warmed HeLa human cervical cancer cells to 39 • C for 24 h and then equilibrated cells back to 37 • C for 30 min prior to infecting with CVB expressing enhanced green fluorescent protein (EGFP-CVB) at a multiplicity of infection of 1 (MOI 1).…”

Inhibition of CaMKII in the Central Nucleus of Amygdala Attenuates Fentanyl-Induced Hyperalgesia in Rats

“…The transient receptor potential vanilloid type 1 (TRPV1) channel, which has been reported to be an essential peripheral mechanism in the expression of morphine-induced hyperalgesia (Vardanyan et al, 2009), is involved in the regulation of synaptic transmission centrally (Shoudai et al, 2010) or peripherally (Sikand and Premkumar, 2007) by enhancing glutamate release from nerve endings (Kaeser and Regehr, 2014;Ramírez-Barrantes et al, 2016). In view of the fact that both TRPV1 mRNA and protein have been found in the central amygdale (Zschenderlein et al, 2011;Ramírez-Barrantes et al, 2016), and that there is evidence for physiologic and pharmacological interactions between CaMKIIa and TRPV1 receptors (Price et al, 2005;Nakanishi et al, 2010) forming possible feed-forward loops , it is therefore possible that presynaptic CaMKIIa may also be a regulator of fentanyl-induced hyperalgesia.…”