TRPV4 contributed to the loss of dopamine neurons and motor deficits in the substantia nigra of PD mice by mediating ER stress and inflammatory pathways.448 Furthermore, activation of TRPV1 channels on astrocytes activated endogenous neuroprotective mechanisms in vivo, which prevented active degeneration of dopamine neurons; this condition led to behavioral recovery via CNTF receptor alpha in nigrostriatal dopamine neurons.449 These studies provide a new perspective on future molecular targets and gene therapies for the treatment of PD. Here, TRPV1 is linked to Parkinson disease.