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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