Abstract
Schizophrenia is characterized by various behavioral abnormalities including cognitive dysfunction. Neonatal ventral hippocampus (NVH)-lesioned rats had been known as neurodevelopmental animal model similar to schizophrenia. Previous observations indicate that postpubertal NVH-lesioned rats exhibit impairments in prepulse inhibition (PPI), spontaneous locomotion, social interaction behavior and working memory. Here, we document the neurochemical basis of those defects in NVH-lesioned rats. Since Ca²⁺/calmodulin-dependent protein kinase II (CaMKII), which is NMDA receptor downstream kinase, is essential for memory and learning acquisition, we developed a protocol to monitor the spatial changes in CaMKII autophosphorylation using immunohistochemical imaging of whole brain slices with anti-autophosphorylated CaMKII antibody in order to address mechanisms underlying impaired cognitive function in NVH-lesioned rats. Immunohistochemical analyses using anti-autophosphorylated CaMKII antibody revealed that CaMKII autophosphorylation was significantly reduced in the medial prefrontal cortex (mPFC) of NVH-lesioned rats compared with control animals. This immunohistochemical technique is useful to investigate temporal and special changes in CaMKII activity in rodent brain and to evaluate drugs to improve the cognitive impairment.
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