Effect of pre- and post-treatment with Bacopa monnieri (Brahmi) on phencyclidine-induced disruptions in object recognition memory and cerebral calbindin, parvalbumin, and calretinin immunoreactivity in rats
Authors Piyabhan P, Tingpej P, Duansak N
Received 3 November 2018
Accepted for publication 5 March 2019
Published 1 May 2019 Volume 2019:15 Pages 1103—1117
Checked for plagiarism Yes
Review by Single anonymous peer review
Peer reviewer comments 3
Editor who approved publication: Dr Yuping Ning
P Piyabhan,1 P Tingpej,2 N Duansak1
1Division of Physiology, Department of Preclinical Science, Faculty of Medicine, Thammasat University, KlongLuang, Pathumthani, Thailand; 2Division of Microbiology, Department of Preclinical Science, Faculty of Medicine, Thammasat University, KlongLuang, Pathumthani, Thailand
Background: Decreased gamma-aminobutyric acid (GABA)-ergic neurons in the brain of both schizophrenic patients and animal models indicates that impairment of GABAergic function is implicated in pathophysiology of the disorder. Decreased GABAergic neurotransmission might be also involved in cognitive impairment, which is developed in schizophrenia. Brahmi (Bacopa monnieri) could be a new treatment and prevention for this cognitive deficit in schizophrenia by increasing GABAergic neurons to a normal level.
Aim: The authors aimed to study cognitive-enhancement- and neuroprotective-effects of Brahmi on novel object recognition memory and GABAergic neuronal density, defined by the presence of calcium binding proteins (CBPs; calbindin (CB), parvalbumin (PV), and calretinin (CR)) in a sub-chronic (2 mg/kg, Bid, ip) phencyclidine (PCP) rat model of schizophrenia.
Materials and methods: In the cognitive-enhancement-effect study rats were assigned to three groups; Group-1: Control, Group-2: PCP-administration, and Group-3: PCP+Brahmi. In the neuroprotective-effect study rats were assigned to three groups; Group-1: Control, Group-2: PCP-administration, and Group-3: Brahmi+PCP. A discrimination ratio (DR) representing cognitive ability was obtained from the novel object recognition task. CB, PV, and CR immunodensity were measured in the prefrontal cortex, striatum, and cornuammonis fields 1–3 (CA1–3) using immunohistochemistry.
Results: Reduced DR was found in the PCP group, which occurred alongside reduced CB, PV, and CR in all brain regions except for CR in the striatum and CA1–3 in the cognitive-enhancement-effect study. PCP+Brahmi showed a higher DR score with increased CB in the prefrontal cortex and striatum, increased PV in the prefrontal cortex and CA1–3, and increased CR in the prefrontal cortex. The Brahmi+PCP group showed higher DR score with increased CB in all areas, increased PV in the striatum, and increased CR in the prefrontal cortex and striatum.
Conclusion: The present study demonstrated the effects, both partial restoration of cognitive deficit and neuroprotection, of Brahmi, and elucidated its underlying mechanism of actions via increasing GABAergic neurons in a PCP-induced schizophrenic-like model.
Keywords: schizophrenia, cognitive impairment, Bacopa monnieri, calbindin, parvalbumin, calretinin
This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution - Non Commercial (unported, v3.0) License. By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms.Download Article [PDF] View Full Text [HTML][Machine readable]