Table 2.

Summarized table of the physiopathological role of GPR3, GPR6 and GPR12.

Target	Physiopathological role	Implication	References
GPR3	Alzheimer’s Disease	Inhibition of amyloid pathology	(Thathiah et al. 2009)
	Multiple Sclerosis	Potential biomarker	(Hecker et al. 2011)
	Neurite Outgrowth	Promotion of neurite outgrowth and cerebellar development	(Tanaka et al. 2014)
	Neuropathic pain	Regulation of neuropathic pain and morphine-induced antinociception	(Ruiz-Medina et al. 2011)
	Cell survival	Induction of neuronal survival and antiapoptotic properties	(Tanaka et al. 2007; Tanaka et al. 2014)
	Stress	GPR3 deletion triggers anxiety-like and depression-like behavior	(Valverde et al. 2009)
	Metabolic Disorders	Impairment of thermogenic response of iBAT and late-onset obesity	(Godlewski et al. 2015)
	Oocyte Maturation	Regulation of meiosis	(Mehlmann et al. 2004)
GPR6	Alzheimer’s Disease	Involvement in the neuroprotective effect of C1q protein	(Benoit et al. 2013)
	Parkinson’s Disease	GPR6 deletion impacts motor symptoms	(Oeckl et al. 2014)
	Huntington’s Disease	GPR6 is downregulated in HD brain	(Hodges et al. 2006)
	Schizophrenia	Impairment of striatum P-DARPP-32	(Oeckl et al. 2014)
	Instrumental learning	Regulation of instrumental performance	(Frank and Fossella 2011; Collins and Frank 2012)
	Cell survival	Antiapoptotic properties	(Ignatov et al. 2003b)
GPR12	Neurite Outgrowth	Promotion of neurite outgrowth	(Tanaka et al. 2007; Tanaka et al. 2014)
	Pain	Sensitivity to heat-related pain	(Carlton et al. 2006)
	Cell survival	Antiapoptotic properties	(Adams and Cory 2007; Lu et al. 2012a; Lu et al. 2012b)
	Cognitive functions	Regulation of long-term memory	(Peters et al. 2008)
	Metabolic Disorders	Appetite control in murine obesity models	(Brennand et al. 2001)
	Oocyte Maturation	Regulation of meiosis (only in rodents)	(Hinckley et al. 2005)