Table 1.

Comparison of reported deficits in MAM GD17 rats with human schizophrenia patients.

Human Schizophrenia	Refs	MAM Rodent Model	Refs
Decrease in medial temporal lobe volume	[34, 76, 78, 79]	Reduced hippocampal volume	[11, 26, 35, 102]
Increased neuronal density in prefrontal areas 9 and 46	[34]	Selective increase in neuronal density in mPFC	[11]
Hippocampal neuronal disarray	[36]	Heterotopias and sporadic neuronal packing in hippocampus	[11, 26, 35]
Sensorimotor gating deficits	[37, 103-105]	Deficit in prepulse inhibition of startle	[11, 26]
Perseveration	[57, 61].	Impaired reversal learning	[11, 44]
Impaired attentional processing	[38, 41, 42].	Deficits in latent inhibition	[44, 45]
Hypersensitivity to drugs that exacerbate positive symptoms	[40, 47]	Enhanced locomotor response to phencyclidine & amphetamine	[11, 35, 53, 99]
Dopamine hyperfunction	[40, 47]	Increased dopamine neuron population activity	[53]
Decreased PV expression in dlPFC and hippocampus	[85]	Decreased PV interneuron number in mPFC and vHipp	[45, 99]
Hypofunctionality of dlPFC and hippocampus by functional imaging studies	[57]	Inability to activate mPFC and vHipp assemblies during a latent inhibition paradigm	[45]
Hippocampal hyperperfusion at rest	[80, 82]	Increased average firing rate of vHipp neurons	[53]
Increased sensitivity to stress	[106]	Stress-induced disruption in mPFC neuronal plasticity	[107]
Working memory deficits	[41, 54-56]	Impaired performance on radial and Y- maze tasks	[11, 26, 44]
Social withdrawal	[108-110]	Decreased social interaction	[26, 35]
Symptoms appear after puberty	[16-20]	Most behavioral deficits emerge post puberty	[11, 26]