Bacopa monnieri (Brahmi) Prevents Cognitive Deficit by Maintaining CA2/3 VGLUT1 Density of Sub-Chronic Phencyclidine Rat Model of Schizophrenia in Normal Level.

Background: 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. Objective: 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. Material and Method: 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 2/3 (CA2/3) and dentate gyrus (DG) of the hippocampus using immunohistochemistry. Results: DR in PCP group was significantly decreased compared with control. This occurred alongside significantly reduced VGLUT1 in prefrontal cortex and CA2/3. 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 CA2/3. Conclusion: Cognitive deficit observed in PCP-administered rats was mediated by VGLUT1 reduction in prefrontal cortex and CA2/3. Interestingly, Brahmi could prevent this cognitive deficit by maintaining VGLUT1 density in CA2/3 in normal level.

Bacopa monnieri (Brahmi) Enhanced Cognitive Function and Prevented Cognitive Impairment by Increasing VGLUT2 Immunodensity in Prefrontal Cortex of Sub-Chronic Phencyclidine Rat Model of Schizophrenia.

BACKGROUND: Glutamatergic hypofunction is affected in schizophrenia. The decrement ofpresynaptic glutamatergic marker remarkably vesicular glutamate transporter type 1 (VGLUT1) indicates the deficit ofglutamatergic and cognitive function in schizophrenic brain. However there have been afew studies in VGLUT2. Brahmi, a traditional herbal medicine, might be a new frontier of cognitive deficit treatment and prevention in schizophrenia by changing cerebral VGLUT2 density. OBJECTIVE: To study cognitive enhancement- and neuroprotective-effects of Brahmi on novel object recognition task and cerebral VGLUT2 immunodensity in sub-chronic phencyclidine (PCP) rat model of schizophrenia. MATERIAL AND METHOD: Cognitive enhancement effect study; rats were assigned to three groups; Group-1: Control, Group-2: PCP administration and Group-3: PCP + Brahmi. Neuroprotective effect study; rats were assigned to three groups; Group-1: Control, Group-2: PCP administration and Group-3: Brahmi + PCP Discrimination ratio (DR) representing cognitive ability was obtained from novel object recognition task. VGLUT2 immunodensity was measured in prefrontal cortex, striatum, cornu ammonis fields 1 (CA1) and 2/3 (CA2/3) of hippocampus using immunohistochemistry. RESULTS: DR was significantly reduced in PCP group compared with control. This occurred alongside VGLUT2 reduction in prefrontal cortex, but not in striatum, CA1 or CA2/3. Both PCP + Brahmi and Brahmi + PCP groups showed an increased DR score up to normal, which occurred alongside a significantly increased VGLUT2 immunodensity in the prefrontal cortex, compared with PCP group. CONCLUSION: The decrement of VGLUT2 density in prefrontal cortex resulted in cognitive deficit in rats receiving PCP. Interestingly, receiving Brahmi after PCP administration can restore this cognitive deficit by increasing VGLUT2 density in prefrontal cortex. This investigation is defined as Brahmi's cognitive enhancement effect. Additionally, receiving Brahmi before PCP administration can also prevent cognitive impairment by elevating VGLUT2 density in prefrontal cortex. This observation indicates neuroprotective effect of Brahmi. Therefore, Brahmi could be a new frontier of restoration and prevention of cognitive deficit in schizophrenia.

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

BACKGROUND: Cognitive deficit is a significant problem, which finally occurs in all schizophrenic patients. It can not be attenuated by any antipsychotic drugs. It is well known that changes of neuronal density are correlated with learning and memory deficits. Bacopa monnieri (Brahmi), popularly known as a cognitive enhancer; might be a novel therapeutic agentfor cognitive deficit in schizophrenia by changing cerebral neuronal density. The objective of this study was to determine the effects of Brahmi on attenuation at cognitive deficit and on the neuronal density in the prefrontal cortex, striatum and cornu ammonis subfield 1 (CA1) and 2/3 (CA2/3) of hippocampus in sub-chronic phencyclidine (PCP) rat model of schizophrenia. MATERIAL AND METHOD: Rats were assigned to three groups; Group-1: Control, Group-2: PCP administration and Group-3: PCP + Brahmi. Rats were testedfor cognitive ability by using the novel object recognition test. Neuronal density from a serial Nissl stain sections ofthe prefrontal cortex, striatum and hippocampus ofrat model ofschizophrenia were measured by using Image ProPlus software and manual counting. RESULTS: Sub-chronic administration of PCP results in cognitive deficits in novel object recognition task. This occurred alongside significantly increased neuronal density in CA1. The cognitive deficit was recovery to normal in PCP + Brahmi group and it occurred alongside significantly decreased neuronal density in CA1. On the other hand, significantly increased neuronal density was observed in CA2/3 of PCP + Brahmi group compared with PCP alone. CONCLUSION: Brahmi is a potential cognitive enhancer against schizophrenia. It reduces neuronal density, most likely glutamatergic neuron, which results in neuronal toxicity and cognitive deficit. Therefore, Brahmi has cognitive enhancement effect by reducing glutamatergic neuron in CAI. Moreover, it also has neurogenesis effect in CA2/3, which is needed to be investigated in the further study.

Neuroprotective effects of Bacopa monnieri (Brahmi) on novel object recognition and NMDAR1 immunodensity in the prefrontal cortex, striatum and hippocampus of sub-chronic phencyclidine rat model of schizophrenia.

BACKGROUND: Cognitive impairment is a major problem, which eventually develops in schizophrenia. It contributes to the patients 'functional disability and cannot be attenuated by antipsychotic drugs. Bacopa monnieri (Brahmi), a neuroprotective herbal medicine in the elderly, might be a novel neuroprotective agent for prevention of cognitive deficit in schizophrenia. OBJECTIVE: To study neuroprotective effects ofBrahmi on novel object recognition task and cerebral glutamate/N-methyl-D- aspartate receptor subtype 1 (NMDAR1) immunodensity in sub-chronic phencyclidine (PCP) rat model ofschizophrenia. MATERIAL AND METHOD: Rats were assigned to three groups; Group-A: Control, Group-B: PCP administration and Group- C: Brahmi + PCP. Discrimination ratio (DR) representing cognitive ability was obtainedfrom novel object recognition task. NMDAR1 immunodensity was measured in prefrontal cortex, striatum, cornu ammonis fields I (CA 1) and 2/3 (CA2/3) and dentate gyrus (DG) using immunohistochemistry. RESULTS: DR was significantly reduced in PCP group compared with control. This occurred alongside NMDAR1 up-regulation in CA2/3 and DG but not in prefrontal cortex, striatum or CA1. Brahmi + PCP group showed an increased DR score up to normal which occurred alongside a significantly decreased NMDARI immunodensity in CA2/3 and DG compared with PCP group. CONCLUSION: Cognitive deficit observed in rats receiving PCP was mediated by NMDAR1 up-regulation in CA2/3 and DG Interestingly, receiving Brahmi before PCP administration can restore this cognitive deficit by decreasingNMDAR1 in these brain areas. Therefore, Brahmi could be a novel neuroprotective agentfor the prevention ofcognitive deficit in schizophrenia.

Cognitive enhancement effects of Bacopa monnieri (Brahmi) on novel object recognition and NMDA receptor immunodensity in the prefrontal cortex and hippocampus of sub-chronic phencyclidine rat model of schizophrenia.

BACKGROUND: Cognitive impairment is a common characteristic in schizophrenia that cannot be attenuated by antipsychotics. Brahmi, popularly known as a cognitive enhancer might be a new frontier of cognitive deficit treatment in schizophrenia. OBJECTIVE: To study effects of Brahmi on attenuation at cognitive deficit and cerebral glutamate/N-methyl-D-aspartate (NMDA) receptor 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 task. NMDA immunodensity was measured in prefrontal cortex, striatum, cornu ammonis fields 1 to 3 of hippocampus (CA1-3), and dentate gyrus (DG) using immunohistochemistry. RESULTS: DR in PCP-group was significantly decreased compared with control. This occurred alongside NMDA up-regulation in prefrontal cortex and CA1-3, but not in striatum and DG. PCP with Brahmi showed a significant increase in DR score compared with PCP alone. This occurred alongside significant decrease in NMDA immunodensity in prefrontal cortex and CA1-3. No significant difference in cerebral NMDA immunodensity was observed between PCP with Brahmi and control. CONCLUSION: Cognitive deficit observed in PCP-administered rats was mediated by NMDA up-regulation in prefrontal cortex and CA1-3. Interestingly, Brahmi could recover this cognitive deficit by decreasing NMDA density in these brain areas to normal.

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.

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.

Withering syndrome in the abalone Haliotis diversicolor supertexta.

Abalone aquaculture is a small but growing industry in Thailand and is based on both the exotic Haliotis diversicolor supertexta and the native H. asinina. Withering syndrome (WS) in abalone is caused by an infection with the Rickettsia-like organism (RLO) 'Candidatus Xenohaliotis californiensis' and has been spread to many countries globally. The present study reports the first observation of the WS-RLO agent in the small abalone, H. diversicolor supertexta in Thailand, Taiwan (ROC) and the People's Republic of China (PRC). Under light microscopy, the RLO was observed as intracytoplasmic inclusions within epithelial cells lining the post-esophagus and, to a minor extent, the intestine of H. diversicolor. Under transmission electron microscopy, inclusions were characterized as colonies of rod-shaped bacteria, 200 x 1800 nm in size, within a vesicle in the cytoplasm of the infected cell. The RLO from the small abalone bound with WS-RLO-specific in situ hybridization probes and was amplified by polymerase chain reaction (PCR), using primers designed from the 16S rDNA sequence of the original WS-RLO from California, USA. The PCR product of RLO samples from both the PRC and Thailand showed extremely high identity with the California WS-RLO (100 and 99%, respectively). These data combined with the history of abalone movements for aquaculture purposes indicate that RLOs observed in Thailand, Taiwan and the PRC are the WS-RLO that originated from California.