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Myelination deficit in a phencyclidine-induced neurodevelopmental model of schizophrenia
Ruiguo Zhang1, Jue He, Shenghua Zhu
1Department 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.
Insights
Schizophrenia may involve problems with myelin, the protective sheath around nerve cells. This study found impaired myelination in a rat model, suggesting a link between myelin dysfunction and schizophrenia development.
Area of Science:
- Neuroscience
- Psychiatry
- Cell Biology
Background:
- Oligodendrocytes produce myelin in the central nervous system.
- Myelination is increasingly implicated in schizophrenia pathogenesis.
- The myelination dysfunction hypothesis requires further investigation.
Purpose of the Study:
- To investigate myelination dysfunction in a phencyclidine (PCP)-induced neurodevelopmental model of schizophrenia.
- To assess the role of oligodendrocytes and myelination in schizophrenia-like behaviors.
Main Methods:
- Rats received daily PCP injections from postnatal day 2.
- Schizophrenia-like behaviors (hyperactivity, prepulse inhibition deficit) were assessed.
- Myelination was measured via myelin basic protein (MBP) expression.
- Mature oligodendrocytes were quantified using glutathione S-transferase (GST)-π expression.
Main Results:
- PCP-treated rats exhibited schizophrenia-like behaviors.
- Reduced MBP expression was observed on postnatal days 16, 22, and 32.
- Decreased GST-π expression was noted on postnatal day 22 in the frontal cortex.
- These findings indicate impaired cerebral myelination.
Conclusions:
- The phencyclidine-induced rat model demonstrates myelination impairment.
- Myelination dysfunction is suggested to play a significant role in schizophrenia pathogenesis.
- Oligodendrocyte dysfunction may be a key factor in schizophrenia development.
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