Pritsana Piyabhan PhD*, Thanitsara Wetchateng PhD*
Affiliation : * Department of Preclinical Science, Faculty of Medicine, Thammasat University, Rangsit Campus, Pathumthani, Thailand
Background : 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.
Objective : To study effects of Brahmi on attenuation at cognitive deficit and cerebral VGLUT1 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 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.
Results : 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.
Conclusion : 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.
Keywords : Brahmi, Schizophrenia, Animal model, Novel object recognition, VGLUT1
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