title: Bacopa monnieri (Brahmi) improved novel object recognition task and increased cerebral vesicular glutamate transporter type 3 in sub-chronic phencyclidine rat model of schizophrenia.
abstract: Reduced vesicular glutamate transporter 1 (VGLUT1) and 2 (VGLUT2) indicate glutamatergic hypofunction leading to cognitive impairment in schizophrenia. However, VGLUT3 involvement in cognitive dysfunction has not been reported in schizophrenia. Brahmi (Bacopa monnieri) might be a new treatment and prevention for cognitive deficits in schizophrenia by acting on cerebral VGLUT3 density. We aimed to study cognitive enhancement- and neuroprotective-effects of Brahmi on novel object recognition and cerebral VGLUT3 immunodensity in sub-chronic (2 mg/kg, Bid, ip) phencyclidine (PCP) rat model of schizophrenia. Rats were assigned to three groups for cognitive enhancement effect study: Group 1, Control; Group 2, PCP administration; Group 3, PCP+Brahmi. A neuroprotective-effect study was also carried out. Rats were again assigned to three groups: Group 1, Control; Group 2, PCP administration; Group 3, Brahmi+PCP. Discrimination ratio (DR) representing cognitive ability was obtained from a novel object recognition task. VGLUT3 immunodensity was measured in the prefrontal cortex, striatum and cornu ammonis fields 1-3 (CA1-3) using immunohistochemistry. We found reduced DR in the PCP group, which occurred alongside VGLUT3 reduction in all brain areas. PCP+Brahmi showed higher DR score with increased VGLUT3 immunodensity in the prefrontal cortex and striatum. Brahmi+PCP group showed a higher DR score with increased VGLUT3 immunodensity in the prefrontal cortex, striatum and CA1-3. We concluded that reduced cerebral VGLUT3 was involved in cognitive deficit in PCP-administrated rats. Receiving Brahmi after PCP restored cognitive deficit by increasing VGLUT3 in the prefrontal cortex and striatum. Receiving Brahmi before PCP prevented cognitive impairment by elevating VGLUT3 in prefrontal cortex, striatum and CA1-3. Therefore, Brahmi could be a new frontier of restoration and prevention of cognitive deficit in schizophrenia.
authors: Division of Physiology, Department of Preclinical Science, Faculty of Medicine, Thammasat University, Klongluang, Pathumthani, Thailand.
authors: Pritsana
authors: P
authors: Piyabhan
authors: Division of Physiology, Department of Preclinical Science, Faculty of Medicine, Thammasat University, Klongluang, Pathumthani, Thailand.
authors: Supaporn
authors: S
authors: Wannasiri
authors: Division of Pharmacology, Department of Preclinical Science, Faculty of Medicine, Thammasat University, Klongluang, Pathumthani, Thailand.
authors: Jarinyaporn
authors: J
authors: Naowaboot
mesh_terms: D000818:Animals; D034681:Bacopa; D001921:Brain / Q000187:drug effects / Q000378:metabolism; D004195:Disease Models, Animal; D008297:Male; D010622:Phencyclidine / Q000008:administration & dosage / Q000633:toxicity*; D010936:Plant Extracts / Q000302:isolation & purification / Q000494:pharmacology / Q000627:therapeutic use*; D051381:Rats; D017208:Rats, Wistar; D021641:Recognition, Psychology / Q000187:drug effects / Q000502:physiology*; D012559:Schizophrenia / Q000139:chemically induced / Q000188:drug therapy / Q000378:metabolism*; D050496:Vesicular Glutamate Transport Proteins / Q000096:biosynthesis*
chemical_list: D010936:Plant Extracts; C482103:Slc17a8 protein, rat; D050496:Vesicular Glutamate Transport Proteins; D010622:Phencyclidine
keywords: VGLUT3; animal model; bacopa monnieri; cognitive impairment; schizophrenia