Bacopa monnieri (Brahmi) Prevents Cognitive Deficit by Maintaining CA23 VGLUT1 Density of Sub-Chronic Phencyclidine Rat Model of Schizophrenia in Normal Level.
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. 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. 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 23 (CA23) and dentate gyrus (DG) of the hippocampus using immunohistochemistry. DR in PCP group was significantly decreased compared with control. This occurred alongside significantly reduced VGLUT1 in prefrontal cortex and CA23. 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 CA23. Cognitive deficit observed in PCP-administered rats was mediated by VGLUT1 reduction in prefrontal cortex and CA23. Interestingly, Brahmi could prevent this cognitive deficit by maintaining VGLUT1 density in CA23 in normal level.