For example, following peripheral nerve lesion that induced neuropathic pain, a neuroimmune response mediated through microglia activation is responsible for loss of inhibition and hyperexcitability51,52 Recent studies suggest that such mechanisms may be responsible for spinal hyperexcitability in PD, as they showed increased cFos activation in the DHSC and increased expression of iba1, a specific marker of microglia activation26,27. Here, FOS is linked to Parkinson disease.