The postweaning social isolation in C57BL/6 mice: preferential vulnerability in the male sex.
Psychopharmacology. 2008-03-04; 197(4): 613-628
DOI: 10.1007/s00213-008-1081-3
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Pietropaolo S(1), Singer P, Feldon J, Yee BK.
Author information:
(1)Laboratory of Behavioural Neurobiology, Swiss Federal Institute of Technology
Zurich, Schorenstrasse 16, CH-8603 Schwerzenbach, Switzerland.
INTRODUCTION: Social deprivation during early life can severely affect mental
health later in adulthood, leading to the development of behavioural traits
associated with several major psychiatric disorders including schizophrenia.
This has led to the application of social isolation in laboratory animals to
model the impact of environmental factors on the aetiopathology of
schizophrenia. However, controversy exists over the precise behavioural profile
and the robustness of some of the reported effects of social isolation rearing.
MATERIALS AND METHODS: Here, we evaluated the efficacy of postweaning social
isolation to induce schizophrenia-related behavioural deficits in C57BL/6 mice
of both sexes.
RESULTS: The effects of social isolation clearly differed between sexes:
isolated male but not female mice exhibited multiple habituation deficits and
enhanced locomotor reaction to amphetamine.
DISCUSSION: The preferential vulnerability in the male sex corresponds well with
the earlier disease onset and poorer prognosis in male relative to female
schizophrenic patients. In contrast, we observed no evidence for a disruption of
sensorimotor gating in the prepulse inhibition paradigm despite the efficacy of
social isolation to alter startle reactivity. With both success and failure in
the induction of schizophrenia-related endophenotypes, the present study thus
provides important characterizations and qualifications to the application of
the social isolation model in mice.
CONCLUSIONS: We conclude that social isolation in mice represents a valuable
tool for the examination of candidate genes within the context of the « two-hit »
hypothesis of the aetiological processes in schizophrenia.