Cognitive enhancement effects of Bacopa monnieri (Brahmi) on novel object recognition and VGLUT1 density in the prefrontal cortex, striatum, and hippocampus of sub-chronic phencyclidine rat model of schizophrenia

Decreased vesicular glutamate transporter type 1 (VGLUT1) in schizophrenic brain indicates the deficit of glutamatergic function, which may produce cognitive impairment in the patients. Brahmi might be a novel therapeutic agent for the cognitive deficit treatment in schizophrenia by changing cerebral VGLUT1 density. To study effects of Brahmi on attenuation at cognitive deficit and cerebral VGLUT1 density in sub-chronic phencyclidine (PCP) rat model of schizophrenia. 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 test. VGLUT1 density was measured in prefrontal cortex, striatum, cornu ammonis fields 1 (CA1) and 2/3 (CA2/3) of hippocampus and dentate gyrus (DG) using western blot and immunohistochemistry. DR in PCP-group was significantly decreased compared with control. This occurred alongside reduced VGLUT1 in prefrontal cortex, striatum, CA1 and CA2/3. PCP with Brahmi showed a significant increase in DR score compared with PCP alone. This occurred alongside significant increase in VGLUT1 in CA1 and CA2/3. Cognitive deficit observed in PCP-administered rats was mediated by VGLUT1 reduction in prefrontal cortex, striatum, CA1 and CA2/3. Interestingly, Brahmi could recover this cognitive deficit by increasing VGLUT1 in CA1 and CA2/3 to normal.