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Brain Res. 2012 Aug 21;1469:136-43. doi: 10.1016/j.brainres.2012.06.003. Epub 2012 Jun 29.

Myelination deficit in a phencyclidine-induced neurodevelopmental model of schizophrenia.

Author information

1
Department of Psychiatry, Xijing Hospital, the Fourth Military Medical University, Xi'an 710032, PR China.

Abstract

Increasing evidence supports an important role of oligodendrocytes and myelination in the pathogenesis of schizophrenia. Oligodendrocytes are the myelin-producing cells in the central nervous system. To test the myelination dysfunction hypothesis of schizophrenia, possible myelination dysfunction was evaluated in a phencyclidine (PCP)-induced neurodevelopmental model of schizophrenia. On postnatal day (PND) 2, rat pups were treated with a total 14 subcutaneous daily injections of PCP (10mg/kg) or saline. PCP-injected rats showed schizophrenia-like behaviors including hyper-locomotor activity on PND 30 and prepulse inhibition deficit on PND 31. Cerebral myelination was measured by the expression of myelin basic protein (MBP), and cerebral mature oligodendrocytes were measured by the expression of glutathione S-transferase (GST)-π in rats. The results indicate that the expressions of MBP on PND 16, 22 and 32 and GST-π on PND 22 decreased in the frontal cortex of PCP-injected rats. Our results suggest that there was myelination impairment in the phencyclidine-induced schizophrenia animal model, and indicate that myelination may play an important role in the pathogenesis of schizophrenia.

PMID:
22750584
DOI:
10.1016/j.brainres.2012.06.003
[Indexed for MEDLINE]

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