It gave a fruit for thought on the scale of work possible from mere observation of natural behaviors of animals (especially fishes in small aquariums). He described the personality traits in fishes and how it influences their cognitive abilities.
Dr. Binoy V.V. , Asst. Professor, School of Natural Sciences and Engineering, NIAS, Bangalore, gave a guest lecture titled "Behavioral syndrome and lateralized utilization of brain hemisphere in an air breathing fish: 'climbing perch'" at Lecture Hall 1, 1st Floor of Administrative Block. It was organised by Prof. Bindu M Kutty.
It gave a fruit for thought on the scale of work possible from mere observation of natural behaviors of animals (especially fishes in small aquariums). He described the personality traits in fishes and how it influences their cognitive abilities.
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Kumaresan (2nd yr MPhil scholar) presented his seminar titled "Nuclear calcium signalling in the regulation of brain function".
Some important discussions:
Vijay Kumar (Senior Research Fellow) presented his seminar on the topic "Cholinergic Transmission in CNS-An Overview". It was very structured: sharing knowledge of cholinergic transmission from the results of various experimetal approaches used, sites of brain involved, disorders implicated, etc.
Some of the important points discussed included the following:
Nesin Mathew (3rd year PhD scholar) presented the progress of her PhD work titled "The role of constraint induced movement therapy (CIMT) in cortical plasticity in animal model of intracortical ischemic stroke".Suwarna Chakraborty (PhD Scholar) presented the paper by Der-Avakian etal from Biological Psychiatry Jan 2014 entitled "Enduring Deficits in Brain Reward Function after Chronic Social Defeat in Rats: Susceptibility,Resilience, and Antidepressant Response"
ABSTRACT Background Anhedonia, or diminished interest or pleasure in rewarding activities, characterizes depression and reflects deficits in brain reward circuitries. Social stress induces anhedonia and increases risk of depression, although the effect of social stress on brain reward function is incompletely understood. Methods This study assessed the following: 1) brain reward function in rats (using the intracranial self-stimulation procedure) and protein levels of brain-derived neurotrophic factor and related signaling molecules in response to chronic social defeat, 2) brain reward function during social defeat and long-term treatment with the antidepressants fluoxetine (5 mg/kg/day) and desipramine (10 mg/kg/day), and 3) forced swim test behavior after social defeat and fluoxetine treatment. Results Social defeat profoundly and persistently decreased brain reward function, reflecting an enduring anhedonic response, in susceptible rats, whereas resilient rats showed no long-term brain reward deficits. In the ventral tegmental area, social defeat, regardless of susceptibility or resilience, decreased brain-derived neurotrophic factor and increased phosphorylated AKT, whereas only susceptibility was associated with increased phosphorylated mammalian target of rapamycin. Fluoxetine and desipramine reversed lower, but not higher, stress-induced brain reward deficits in susceptible rats. Fluoxetine decreased immobility in the forced swim test, as did social defeat. Conclusions These results suggest that the differential persistent anhedonic response to psychosocial stress may be mediated by ventral tegmental area signaling molecules independent of brain-derived neurotrophic factor and indicate that greater stress-induced anhedonia is associated with resistance to antidepressant treatment. Consideration of these behavioral and neurobiological factors associated with resistance to stress and antidepressant action may promote the discovery of novel targets to treat stress-related mood disorders. Kumaresan UD (MPhil Scholar) presented the paper by Zhan et al in Nature Neuroscience entitled "Deficient neuron-microglia signaling results in impaired functional brain connectivity and social behavior"
ABSTRACT Microglia are phagocytic cells that infiltrate the brain during development and have a role in the elimination of synapses during brain maturation. Changes in microglial morphology and gene expression have been associated with neurodevelopmental disorders. However, it remains unknown whether these changes are a primary cause or a secondary consequence of neuronal deficits. Here we tested whether a primary deficit in microglia was sufficient to induce some autism-related behavioral and functional connectivity deficits. Mice lacking the chemokine receptor Cx3cr1 exhibit a transient reduction of microglia during the early postnatal period and a consequent deficit in synaptic pruning. We show that deficient synaptic pruning is associated with weak synaptic transmission, decreased functional brain connectivity, deficits in social interaction and increased repetitive-behavior phenotypes that have been previously associated with autism and other neurodevelopmental and neuropsychiatric disorders. These findings open the possibility that disruptions in microglia-mediated synaptic pruning could contribute to neurodevelopmental and neuropsychiatric disorders. |
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August 2019
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