Table 1.

Several animal models have studied schizophrenia.

		MAM	NVHL
Executive functions	Attentional processes	Flagstad et al., 2005; Featherstone et al., 2007
	Working memory deficits	Flagstad et al., 2005; Hazane et al., 2009	Chambers et al., 1996; Lipska et al., 2002
	Perseveration	Moore et al., 2006; Hazane et al., 2009	Marquis et al., 2008
	Recognition deficits	Featherstone et al., 2007	Sams-Dodd et al., 1997; Bachevalier et al., 1999
Motivational behavior	Increased liability for addictive behaviors	Flagstad et al., 2005	Swerdlow et al., 2001; Brady et al., 2008
	Responses to stress	Le Pen et al., 2006; Hazane et al., 2009	Sams-Dodd et al., 1997
Activity	Hyperlocomotion	Le Pen et al., 2006; Moore et al., 2006; Penschuck et al., 2006; Hazane et al., 2009	Lipska et al., 1993; Wan et al., 1996
Information filtering mechanism	Sensorimotor gating deficits	Le Pen et al., 2006; Moore et al., 2006; Hazane et al., 2009	Swerdlow et al., 1995

Pharmacological models have used amphetamine, PCP or NMDA to simulate some of the symptoms. However, only two models have shown the illness as a developmental process. The neonatal ventral hippocampal lesion (NVHL) and MAM models showed marked maladaptive behavior when animals reached adulthood. Le Pen et al. (2011) and O’Donnell (2011) have described several behavioral procedures where we can find similar results with different techniques aimed at developing a dysfunctional PfC.