Table 1.

Cellular, neurotransmitter, circuitry, and behavioral deficits in Disc1 mouse models

		Haploinsufficiency	Point mutation	Dominant-negative
Cellular	Early developmental deficits		↓ (Lee et al., 2011)
	Trafficking	↓ (Tsuboi et al., 2015)
	Oxidative stress			↑ (Johnson et al., 2013)
	Ca2+ signaling	↑ (Park et al., 2015)
	Neural plasticity			↓ (Greenhill et al., 2015)
Neurotransmitter	Dopaminergic	↑ (Nakai et al., 2014)	↑ (Su et al., 2014)	↑ (Jaaro-Peled et al., 2013; Kim et al., 2015)
	Glutamatergic			↓ (Booth et al., 2014; Dawson et al., 2015; Kim et al., 2015)
	GABAergic	↓ (Nakai et al., 2014)
	Cannabinoid			↓ (Kaminitz et al., 2014; Ballinger et al., 2015; Kim et al., 2015)
	Nicotinic			↓ (Kim et al., 2015)
Circuitry	Local circuitry (Hippocampus)	↓ (Kvajo et al., 2011)
	Long-range circuitry (Mesocortical circuit)			↓ (Niwa et al., 2013)
Behavior	Sensitivity to psychostimulants		↑ (Clapcote et al., 2007)	↑ (Jaaro-Peled et al., 2013)
	Prepulse inhibition		↓ (Clapcote et al., 2007)	↓ (Hikida et al., 2007)
	Working memory	↓ (Koike et al., 2006)	↓ (Clapcote et al., 2007)
		Sociability	↓ (Clapcote et al., 2007)	↓ (Johnson et al., 2013)
	Depressive like		↑ (Clapcote et al., 2007)	↑ (Hikida et al., 2007)