Background: Decreased vesicular glutamate transporter type 1 (VGLUT1) has been reported in the brains of both postmortem and animal models of schizophrenia. It indicates the deficit of glutamatergic function which is implicated in the cognitive deficit in schizophrenia. Our previous study investigated that Brahmi can recover the cognitive deficit in schizophrenia by upregulating cerebral VGLUT1 density. However, the neuroprotective effects of Brahmi have not been studied yet.
Objective: To study the effects of Brahmi on the prevention of cognitive deficit and cerebral VGLUT1 density in sub-chronic phencyclidine (PCP) rat model of schizophrenia.
Material and Method: Rats were assigned to three groups; Group-A: Control, Group-B: PCP administration and Group-
C: Brahmi + PCP. Cognitive ability was represented by the Discrimination ratio (DR) calculated from novel object recognition test. VGLUT1 optical density was measured in prefrontal cortex, striatum, cornu ammonis fields 1 (CA1) and 2/3 (CA2/3) and dentate gyrus (DG) of the hippocampus using immunohistochemistry.
Results: DR in PCP group was significantly decreased compared with control. This occurred alongside significantly reduced VGLUT1 in prefrontal cortex and CA2/3. Brahmi + PCP group showed a significant increase in DR score compared with PCP alone; however, it was still lower than control. This occurred alongside significant increase in VGLUT1 in CA2/3.
Conclusion: Cognitive deficit observed in PCP-administered rats was mediated by VGLUT1 reduction in prefrontal cortex
and CA2/3. Interestingly, Brahmi could prevent this cognitive deficit by maintaining VGLUT1 density in CA2/3 in normal level.

Keywords: Brahmi, Schizophrenia, Animal models, Novel object recognition, VGLUT1