In an in vivo study with a mice model of HD, BACHD, in which there is high expression levels of neuropathogenic, full length mutant huntingtin (fl-mHTT) genes, lower expression of GPR88 has been found in the striatum, that is accompanied by hyperexcitability, increased amplitude of AMPA receptor-mediated synaptic and a decline in spine density (Rocher et al., 2016). This evidence concerns the gene HTT and Huntington disease.