Pritsana Piyabhan PhD*, Thanitsara Wetchateng PhD*, Seewaboon Sireeratawong PhD*
Affiliation : * Department of Preclinical Science, Faculty of Medicine, Thammasat University, Rangsit Campus, Pathumthani, Thailand
Background : Cognitive impairment is a common characteristic in schizophrenia that cannot be attenuated by antipsychotics.
Brahmi, popularly known as a cognitive enhancer, might be a new frontier of cognitive deficit treatment in schizophrenia.
Objective : To study effects of Brahmi on attenuation at cognitive deficit and cerebral glutamate/N-methyl-D-aspartate
(NMDA) receptor density in sub-chronic phencyclidine (PCP) rat model of schizophrenia.
Material and Method: Rats were administered PCP or vehicle. Half of the PCP-group was treated with Brahmi.
Discrimination ratio (DR) representing cognitive ability was obtained from novel object recognition task. NMDA
immunodensity was measured in prefrontal cortex, striatum, cornu ammonis fields 1 to 3 of hippocampus (CA1-3), and
dentate gyrus (DG) using immunohistochemistry.
Results : DR in PCP-group was significantly decreased compared with control. This occurred alongside NMDA up-regulation
in prefrontal cortex and CA1-3, but not in striatum and DG. PCP with Brahmi showed a significant increase in DR score
compared with PCP alone. This occurred alongside significant decrease in NMDA immunodensity in prefrontal cortex and
CA1-3. No significant difference in cerebral NMDA immunodensity was observed between PCP with Brahmi and control.
Conclusion : Cognitive deficit observed in PCP-administered rats was mediated by NMDA up-regulation in prefrontal cortex
and CA1-3. Interestingly, Brahmi could recover this cognitive deficit by decreasing NMDA density in these brain areas to
normal.
Keywords : Brahmi, Schizophrenia, Animal model, Novel object recognition, NMDA receptor
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