Table 1. Recent studies using behavioral paradigms that measure positive symptoms of schizophrenia in rodent models.

Paradigm	Animal Model	Experimental Manipulation	Results	References
Open field test	Developmental	Poly(I:C)-induced MIA mouse offspring	↑ increased locomotion	[45]
		Perinatal L-Dopa treatment in female juvenile mice	↑ increased locomotion	[46]
	Genetic	SREBP1c KO mice	↑ increased locomotion	[47]
		GPR88 KO mice	↑ increased locomotion	[48]
		Dtnbp1 deficient mice	↑ increased locomotion	[49]
		mGlu5 KO mice	↑ increased locomotion	[50]
		NMDA receptor ablated mice	↑ increased locomotion	[51]
		Brain-specific CRMP2 KO mice	↑ increased locomotion	[52]
		Df(h1q21)/+ mice (1q21.1 hemizygous microdeletion)	↑ increased locomotion	[53]
		DAT KO mice	↑ increased locomotion	[54]
		GLAST KO mice	↑ increased locomotion	[55]
		Reduced SLC1A1 expression in mice	NE	[56]
		GAS7 deficient mice	NE	[57]
		Type III NRG1+/− male mice from the mutant fathers	NE	[58]
		Selective mPFC PLC-β1 knockdown mice	NE	[59]
	Pharmacological	Amphetamine (1 and 5 mg/kg) or MK-801 (0.01 and 0.05 mg/kg),Higher doses of amphetamine (25 mg/kg) or MK-801 (0.25 mg/kg) administration in mice	↑ increased locomotionNE	[23]
		Administration of Catha edulis forsk extract in mice	↑ increased locomotion	[60]
		hM4D-mediated inhibition of GAD65 interneurons in the mouse vHPC	↑ increased locomotion	[61]
		PCP + Δ9-THC treated mice	↑ increased locomotion	[62]
Prepulse inhibition	Developmental	Poly(I:C)-induced MIA mouse offspring	↓ decreased inhibition	[70]
	Genetic	SREBP1c KO mice	↓ decreased inhibition	[47]
		NAc-TMEM mice	↓ decreased inhibition	[80]
		GPR88 KO mice	↓ decreased inhibition	[48]
		Dtnbp1 deficient mice	↓ decreased inhibition	[49]
		Df(h1q21)/+ mice (1q21.1 hemizygous microdeletion + amphetamine)	↓ decreased inhibition	[53]
		Chakragati mice	↓ decreased inhibition	[72]
		mGlu5 KO mice	↓ decreased inhibition	[50]
		GAS7 deficient mice	↓ decreased inhibition	[57]
		DAT KO mice	↓ decreased inhibition	[54]
		Nlgn2 R215H KI homozygous mice	↑ increased inhibition	[73]
		Selective mPFC PLC-β1 knockdown mice	NE	[59]
		Type III NRG1+/−□male mice from mutant fathers	NE	[58]
		Reelin-deficient + corticosterone-treated mice	NE	[71]
	Pharmacological	hM4D-mediated inhibition of parvalbumin interneurons in the mouse vHPC	↓ decreased inhibition	[61]
		PCP+ Δ9-THC treated mice	↓ decreased inhibition	[62]
		hM4D-mediated inhibition of GAD65 interneurons in the mouse vHPC	NE	[61]

Abbreviations: CRMP2 = collapsin response mediator protein 2; DAT = dopamine transporter; Dtnbp1 = dystrobrevin binding protein; GAD65 = glutamic acid decarboxylase 65; GAS7 = growth arrest-specific 7; GLAST = glial glutamate and aspartate transporter; GPR88 = G protein-coupled receptor 88; KO = knockout; L-dopa = levodopa; mGluR5 = metabotropic glutamate receptor 5 = MIA, maternal immune activation; mPFC = medial prefrontal cortex; NAc-TMEM mice = Tmem168 vector was injected into the NAc of C57BL/6J mice; Nlgn2 R215H = missense mutation R215H of neuroligin 2; NMDA = N-methyl-D-aspartate; NRG1 = neuregulin-1; PCP = phencyclidine; PLC-β1 = phospholipase C-β1; poly(I:C) = polyinosinic-polycytidylic acid; SLC1A1 = Solute Carrier Family 1 Member 1; SREBP1c = sterol regulatory element-binding protein 1c; vHPC = ventral hippocampus; Δ9-THC = Δ9-tetrahydrocannabinol; NE = no effect.