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Adolescence is a critical period for the development of neural plasticity. Social isolation is an important animal model for various neurodevelopmental disorders. Brain derived neurotrophic factor (BDNF) mediates many important brain functions such as neural plasticity, and aberrations in its expression have been implicated in many brain disorders. However, to date there have been few reports of effects of adolescent social isolation on BDNF expression in adult animals. In the present study, we subjected weaning Sprague Dawley rats to a four-week early adolescence social isolation procedure followed by four-week standard housing until adulthood for molecular assays. BDNF protein levels in several key forebrain regions relevant to brain development were investigated using immunohistochemistry, including frontal and cingulate cortex as well as hippocampus. Our results show that adolescent social isolation significantly increased BDNF protein expression in the medial prefrontal cortex and all three sub-fields of the hippocampus, including CA1, CA2/3 and dentate gyrus. This study advances the use of adolescent social isolation as an animal model for studying neurobiological underpinnings of various neurodevelopmental disorders., (Copyright © 2010 Elsevier B.V. All rights reserved.)

Puberty is a critical period for neurodevelopment of schizophrenia. In the present study, we investigated the effects of peri-pubertal social isolation on psychotic behaviors in rats and its relationship to dopamine expression. Wistar male rats were randomly divided into pubertal isolation (ISO; isolate housing, 38-51 days of age) and social (SOC) groups. Latent inhibition (LI) and behavior in open field were tested during adolescence and adulthood. After the behavioral test, dopamine (DA) levels were measured in the medial prefrontal cortex (mPFC), nucleus accumbens (NAC), caudate-putamen (CPU), and the hippocampus (HIP). Pubertal social isolation impaired LI and increased the DA level in the NAC of young adult rats, but not adolescent rats, and enhanced open field locomotor activity in both adolescent and young adult rats. These data suggest that development of an LI deficit can be induced by social isolation during puberty after a developmental delay, and that NAC DA maybe involved in this process, which may mirror some aspects of the ontogency of schizophrenic symptoms.