Skip to main content
. Author manuscript; available in PMC: 2011 Dec 15.
Published in final edited form as: Biol Psychiatry. 2010 Dec 15;68(12):1172–1181. doi: 10.1016/j.biopsych.2010.09.022

Table 1.

The summary of the effects of gene-environment interactions

Test Outcomes Possible interpretations
Affective behaviors
Open field test - peripheral zone
Elevated plus maze – open arms
Forced swim test - immobility
Tail suspension test - immobility
Sociability test – sniffing time

Increased
Decreased
Increased
Increased
Decreased

The effects in these tests suggest increased anxiety and depression-like phenotypes, consistent with aspects of mood disorders
Learning and memory
Spontaneous alternation
Spatial recognition in Y maze
Morris water maze
Object recognition test

Unaffected
Unaffected
Unaffected
Unaffected
These tests evaluate cognitive changes in mice. The lack of the significant effects in the tests may indicate no effects on learning and memory
Sensory-motor integration
Pre-pulse inhibition of the acoustic startle

Unaffected
This test evaluates sensory--motor gating processing in mice
Brain pathology
Lateral ventricles enlargement

Brain region volumes
 - Amygdala
 - Hypothalamus
 - PAGM
 - Cortex
 - Hippocampus
 - Striatum

Spine density in the hippocampus

Attenuated


Decreased
Decreased
Decreased
Unaffected
Unaffected
Unaffected

Decreased

The brain abnormalities may explain the affective phenotypes and seem to be consistent with brain pathological findings in patients with mood disorders
Neurochemical changes
 - Dopamine
 - Norepinephrine
 - Serotonin
 - DA metabolism
 - 5-HT metabolism

Unaffected
Unaffected
Increased
Unaffected
Decreased
Attenuated 5-HT neurotransmission may contribute to the behavioral phenotypes in mice and appears in line with alterations found in affective disorders
Molecular markers
 - Mutant DISC1
 - Endogenous DISC1

 - GSK-3β

Increased
Decreased

Unaffected by poly I:C stimulation in mutant DISC1 mice
Altered expression of DISC1 and its interactors may underlie the brain abnormalities in mice

GSK-3β is a key DISC1 partner and a main factor of the immune signaling. Abnormal interaction between GSK-3β and DISC1 could contribute to altered cytokine production in mhDISC1 mice