BHAGYA VENKANNA RAO
@klepharmblr.org
Associate Professor Department of Pharmacology
KLE College of Pharmacy, KAHER, Bengaluru
Publications
1. V Bhagya, BN Srikumar, TR Raju and BS Shankaranarayana Rao (2008) Neonatal clomipramine induced endogenous depression in rats is associated with learning impairment in adulthood. Behavioural Brain Research 187: 190–194
2. Veena J, Srikumar BN, Mahati K, Bhagya V, Raju TR and Shankaranarayana Rao BS (2009) Enriched environment restores hippocampal cell proliferation and ameliorates cognitive deficits in chronically stressed rats. Journal of Neuroscience Research 87: 831–843
3. George Lekha, Bhagya P Kumar, Shankar Narayana Rao, Irudaya Arockiasamy and Karthik Mohan (2010) Cognitive enhancement and Neuroprotective effect of Celastrus paniculatus Willd. seed oil (Jyothismati oil) on male Wistar rats. Journal of Pharmaceutical Science and Technology 2(2): 130-138
4. Bhagya V, Srikumar BN, Raju TR, Shankaranarayana Rao BS (2011) Chronic escitalopram treatment restores spatial learning, monoamine Levels and hippocampal long term potentiation in an animal model of depression.
EDUCATION
M Pharm (Pharmacology)
PhD (Neurophysiology)
RESEARCH INTERESTS
Neuronal Plasticity
Psychiatric disorders
Herbal remedies
Scopus Publications
Scholar Citations
Scholar h-index
Scholar i10-index
Scopus Publications
Dhruti Avlani, H.N. Shivakumar, Avichal Kumar, A. Prajila, Babiker Bashir Haroun Baraka, and V. Bhagya
Elsevier BV
Shankaranarayana Rao
CSIR-National Institute of Science Communication and Policy Research (NIScPR)
Neuronal plasticity is enhanced in an enriched environment (EE) with more sensory and social interaction. In an animal model of endogenous depression, we have previously shown that EE has positive effects on spatial memory and hippocampus synaptic plasticity. However, nothing is known about how EE influences dendritic remodelling in hippocampal neurons affected by endogenous depression. In depressed rats, the impact of EE on hippocampus neuronal morphology was examined. Neonatal clomipramine exposure from postnatal days (PND) 8-21 days induced endogenous depression. The depressed-like rats were exposed to an enriched environment for two weeks in adulthood. Brains were then collected, stained with a modified Golgi-cox technique and, the hippocampal CA1 dendritic arborisation was evaluated using the Neurolucida software. Depression resulted in the atrophy of CA1 hippocampal neurons. The number of branching points and the overall number of dendritic intersections were reduced in depressed rats,. Exposure to an enriched environment significantly increased dendritic branching and the total number of dendritic intersections in hippocampal CA1 pyramidal neurons. The hippocampal pyramidal neuronal morphology of depressed rats improved after exposure to environmental enrichment. Neuronal plasticity and the development of novel therapeutic strategy will be improved by a greater understanding of how the environment affects neuronal morphology in depressed states.
S. Abhijit, Sunil Jamuna Tripathi, V. Bhagya, B.S. Shankaranarayana Rao, Muthangi V. Subramanyam, and S. Asha Devi
Elsevier BV
Venkanna Rao Bhagya, Bettadapura N. Srikumar, Jayagopalan Veena, and Byrathnahalli S. Shankaranarayana Rao
Wiley
Exposure to prolonged stress results in structural and functional alterations in the hippocampus including reduced long‐term potentiation (LTP), neurogenesis, spatial learning and working memory impairments, and enhanced anxiety‐like behavior. On the other hand, enriched environment (EE) has beneficial effects on hippocampal structure and function, such as improved memory, increased hippocampal neurogenesis, and progressive synaptic plasticity. It is unclear whether exposure to short‐term EE for 10 days can overcome restraint stress–induced cognitive deficits and impaired hippocampal plasticity. Consequently, the present study explored the beneficial effects of short‐term EE on chronic stress–induced impaired LTP, working memory, and anxiety‐like behavior. Male Wistar rats were subjected to chronic restraint stress (6 hr/day) over a period of 21 days, and then they were exposed to EE (6 hr/day) for 10 days. Restraint stress reduced hippocampal CA1‐LTP, increased anxiety‐like symptoms in elevated plus maze, and impaired working memory in T‐maze task. Remarkably, EE facilitated hippocampal LTP, improved working memory performance, and completely overcame the effect of chronic stress on anxiety behavior. In conclusion, exposure to EE can bring out positive effects on synaptic plasticity in the hippocampus and thereby elicit its beneficial effects on cognitive functions. © 2016 Wiley Periodicals, Inc.
BM Shilpa, V Bhagya, G Harish, MM Srinivas Bharath, and BS Shankaranarayana Rao
Elsevier BV
V Bhagya, Thomas Christofer, and BS Shankaranarayana Rao
Medknow
Objective: Several studies report that chronic stress results in impaired spatial learning and working memory and enhanced anxiety-like behavior. However, not many studies have looked into the possible ways of reversing stress-induced deficits. Celastrus paniculatus (CP), a traditional ayurvedic herbal medicine, was used to treat cognitive deficits in mentally retarded children. CP oil has been reported to have neuroprotective and antioxidant activities. However, the effects of CP oil on chronic stress-induced cognitive deficits are unclear. In the present study, we intended to analyze the neuroprotective effects of CP oil on stress-associated cognitive dysfunctions. Materials and Methods: Chronic stress was induced by subjecting rats to restrainers for 6 h a day for 21 days. CP oil (400, 600 mg/kg) or vehicle was administered intraperitoneally (i.p.) after stress protocol once a day over the next 14 days. Groups used in the present study: normal control, stress, stress + vehicle, stress + CP oil at 2 different doses (400 and 600 mg/kg, i.p.). After the drug treatment, open field and elevated plus maze (EPM) were used to analyze anxiety-like behavior, and partially baited radial arm maze (RAM) and T-maze were used to evaluate spatial learning and memory capabilities. Analysis has been done using two-way ANOVA followed by Bonferroni's post hoc test and one-way ANOVA followed by Tukey's post hoc test. Results: Stressed rats showed enhanced anxiety-like behavior in EPM (P < 0.001) and impaired performance in RAM (P < 0.001) and T-maze tasks (P < 0.001) compared to normal animals. In contrast, CP oil treatment to these rats improved their performance in both RAM (P < 0.001) and T-maze (P < 0.001). In addition, CP oil significantly reduced stress-induced anxiety behavior (P < 0.001). Conclusion: Chronic treatment with CP oil is to improve cognitive abilities in chronically stressed rats. The current study provides a novel perspective on beneficial effect of herbal therapy on stress-induced cognitive dysfunctions.
K. Mahati, V. Bhagya, T. Christofer, A. Sneha, and B.S. Shankaranarayana Rao
Elsevier BV
V. Bhagya, B.N. Srikumar, T.R. Raju, and B.S. Shankaranarayana Rao
Wiley
Depression is a major psychiatric illness that is associated with cognitive dysfunctions. The underlying mechanism of depression‐associated memory impairment is unclear. Previously, we showed altered hippocampal synaptic plasticity in an animal model of depression. Although several antidepressants are beneficial in the treatment of depression, very little is known about the effects of these drugs on depression‐associated learning and memory deficits. Prolonged antidepressant treatment might contribute to neuroplastic changes required for clinical outcomes. Accordingly, we evaluated the effect of chronic reboxetine (a selective noradrenergic reuptake inhibitor) treatment on depression‐induced reduced hippocampal synaptic plasticity, neurotransmitter levels, and spatial learning and memory impairments. Depression was induced in male Wistar rats by the administration of clomipramine from postnatal days 8 to 21, and these rats were treated with reboxetine in adulthood. The neonatal clomipramine administration resulted in impaired hippocampal long‐term potentiation (LTP), decreased hippocampal cholinergic activity and monoamine levels, and poor performance in a partially baited eight‐arm radial maze task. Chronic reboxetine treatment restored the hippocampal LTP, acetylcholinesterase activity, and levels of biogenic amines and ameliorated spatial learning and memory deficits in the depressed state. Thus, restoration of hippocampal synaptic plasticity might be a cellular mechanism underlying the beneficial effect of reboxetine in depression‐associated cognitive deficits. This study furthers the existing understanding of the effects of antidepressants on learning, memory, and synaptic plasticity and could ultimately assist in the development of better therapeutic strategies to treat depression and associated cognitive impairments. © 2014 Wiley Periodicals, Inc.
V. Bhagya, B. N. Srikumar, T. R. Raju, and B. S. Shankaranarayana Rao
Springer Science and Business Media LLC
RationaleThe neural basis of depression-associated cognitive impairment remains poorly understood, and the effect of antidepressants on learning and synaptic plasticity in animal models of depression is unknown. In our previous study, learning was impaired in the neonatal clomipramine model of endogenous depression. However, it is not known whether the cognitive impairment in this model responds to antidepressant treatment, and the electrophysiological and neurochemical bases remain to be determined.ObjectivesTo address this, we assessed the effects of escitalopram treatment on spatial learning and memory in the partially baited radial arm maze (RAM) task and long-term potentiation (LTP) in the Schaffer collateral-CA1 synapses in neonatal clomipramine-exposed rats. Also, alterations in the levels of biogenic amines and acetylcholinesterase (AChE) activity were estimated.ResultsFourteen days of escitalopram treatment restored the mobility and preference to sucrose water in the forced swim and sucrose consumption tests, respectively. The learning impairment in the RAM was reversed by escitalopram treatment. Interestingly, CA1-LTP was decreased in the neonatal clomipramine-exposed rats, which was restored by escitalopram treatment. Monoamine levels and AChE activity were decreased in several brain regions, which were restored by chronic escitalopram treatment.ConclusionsThus, we demonstrate that hippocampal LTP is decreased in this animal model of depression, possibly explaining the learning deficits. Further, the reversal of learning and electrophysiological impairments by escitalopram reveals the important therapeutic effects of escitalopram that could benefit patients suffering from depression.
J. Veena, B. N. Srikumar, K. Mahati, V. Bhagya, T. R. Raju, and B. S. Shankaranarayana Rao
Wiley
Adult neurogenesis, particularly in the subgranular zone, is thought to be linked with learning and memory. Chronic stress inhibits adult hippocampal neurogenesis and also impairs learning and memory. On the other hand, exposure to enriched environment (EE) is reported to enhance the survival of new neurons and improve cognition. Accordingly, in the present study, we examined whether short‐term EE after stress could ameliorate the stress‐induced decrease in hippocampal cell proliferation and impairment in radial arm maze learning. After restraint stress (6 hr/day, 21 days) adult rats were exposed to EE (6 hr/day, 10 days). We observed that chronic restraint stress severely affected formation of new cells and learning. Stressed rats showed a significant decrease (70%) in the number of BrdU (5‐bromo‐2′‐deoxyuridine)‐immunoreactive cells and impairment in the performance of the partially baited radial arm maze task. Interestingly, EE after stress completely restored the hippocampal cell proliferation. On par with the restoration of hippocampal cytogenesis, short‐term EE after stress resulted in a significant increase in percentage correct choices and a decrease in the number of reference memory errors compared with the stressed animals. Also, EE per se significantly increased the cell proliferation compared with controls. Furthermore, stress significantly reduced the hippocampal volume that was reversed after EE. Our observations demonstrate that short‐term EE completely ameliorates the stress‐induced decrease in cell proliferation and learning deficit, thus demonstrating the efficiency of rehabilitation in reversal of stress‐induced deficits and suggesting a probable role of newly formed cells in the effects of EE. © 2008 Wiley‐Liss, Inc.
V. Bhagya, B.N. Srikumar, T.R. Raju, and B.S. Shankaranarayana Rao
Elsevier BV
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Publications
Publications
1. V Bhagya, BN Srikumar, TR Raju and BS Shankaranarayana Rao (2008) Neonatal clomipramine induced endogenous depression in rats is associated with learning impairment in adulthood. Behavioural Brain Research 187: 190–194
2. Veena J, Srikumar BN, Mahati K, Bhagya V, Raju TR and Shankaranarayana Rao BS (2009) Enriched environment restores hippocampal cell proliferation and ameliorates cognitive deficits in chronically stressed rats. Journal of Neuroscience Research 87: 831–843
3. George Lekha, Bhagya P Kumar, Shankar Narayana Rao, Irudaya Arockiasamy and Karthik Mohan (2010) Cognitive enhancement and Neuroprotective effect of Celastrus paniculatus Willd. seed oil (Jyothismati oil) on male Wistar rats. Journal of Pharmaceutical Science and Technology 2(2): 130-138
4. Bhagya V, Srikumar BN, Raju TR, Shankaranarayana Rao BS (2011) Chronic escitalopram treatment restores spatial learning, monoamine Levels and hippocampal long term potentiation in an animal model of depression. Psychopharamcology (Berl) 214:477–494
5. Bhagya V, Srikumar BN, Raju TR, Shankaranarayana Rao BS (2015) Selective noradrenergic reuptake inhibitor reboxetine restores spatial learning deficits, biochemical changes and hippocampal synaptic plasticity in an animal model of depression. Journal of Neuroscience Research 93: 104-120
6. Bhagya V*, Christofer T, Shankaranarayana Rao BS (2016) Neuroprotective effect of Celastrus paniculatus on chronic stress-induced cognitive impairment. Indian J Pharmac