Jyothi Prasad (Research Fellow) presented her seminar on "Animal Models of Parkinson's Disease".
Ajay Nair (3rd year PhD Scholar) presented the paper by MM Arnold etal from Journal of Sleep Research, 2013 entitled "Information content in cortical spike trains during brain state transitions"
Even in the absence of external stimuli there is ongoing activity in the cerebral cortex as a result of recurrent connectivity. This paper attempts to characterize one aspect of this ongoing activity by examining how the
information content carried by specific neurons varies as a function of brain state. We recorded from rats chronically implanted with tetrodes in the primary visual cortex during awake and sleep periods. Electroencephalogram and spike trains were recorded during 30-min periods, and 2–4 neuronal spikes were isolated per tetrode off-line.
All the activity included in the analysis was spontaneous, being recorded from the visual cortex in the absence of visual stimuli. The brain state was determined through a combination of behavior evaluation, electroencephalogram
and electromyogram analysis. Information in the spike trains was determined by using Lempel–Ziv Complexity. Complexity was used to estimate the entropy of neural discharges and thus the information content (Amigo´ et al. Neural Comput., 2004, 16: 717–736).
The information content in spike trains (range 4–70 bits s)1) was evaluated during different brain states and particularly during the transition periods. Transitions toward states of deeper sleep coincided with a decrease of information, while transitions to the awake state resulted in an increase in information. Changes in both directions were of the same magnitude, about 30%. Information in spike trains showed a high temporal correlation between neurons, reinforcing the idea of the impact of the brain state in the information content of spike trains.
Kala P Nair (1st year MPhil scholar) presented the paper by Yamaguchi etal from Neuron 2013 entitled "Distinct Roles of Segregated Transmission of the Septo-Habenular Pathway in Anxiety and Fear"
The posterior septum consisting of the triangular septum (TS) and the bed nucleus of the anterior commissure (BAC) is predominantly linked with the medial habenula (MHb) and has been implicated in the control of anxiety and fear responses. However, its anatomical and functional linkage has largely remained elusive. We established a transgenic mouse model in which the TS and BAC projection neurons were visualized by GFP fluorescence and selectively eliminated by immunotoxin-mediated cell targeting.
The linkage between the TS/BAC and the MHb constitutes two parallel pathways composed of the TS-ventral MHb, the core part of the interpeduncular nucleus (IPN), and the BAC-dorsal MHb, the peripheral part of the IPN. Ablation of the TS and BAC projection neurons selectively impaired anxiety and enhanced fear responses and learning, respectively. Inputs from the TS and BAC to the MHb are thus segregated by two parallel pathways and play
specialized roles in controlling emotional behaviors.
Abhilash PL (1st year PhD scholar) presented his seminar on "Astrocytes in neurodegenerative diseases".
After a brief introduction of the morphology and classification of astrocytes (broadly protoplasmic - with short 30 micron processes and fibrous with 300 micron long processes), Abhilash went over the GFAP (expressed more during reactive astrogliosis) and S100Beta (Ca binding protein that gets expressed more during injury) expression and then came to the various functional roles of astrocytes.
Astrocytes have a significant role in the lifespan of synapse formation (from birth to death of synapes) and interestingly, under healthy conditions they maintain own territorial domains with less than 5% of overlap between astrocyte processes. Through the astrocytic gap junctions, K+ buffering and Ca+ wave propogation take place. In the tripartite synapse, only 20% of the glutamate released is taken up by the postsynaptic terminal with 80% of it being cleared up by astrocytes. Astrocytes are also involved in Glutathione synthesis and produce precursers that allow neurons to also manufacture Glutathione (as they can't take in Glutathione from extracellular space).
Astrocytes are implicated in neurodegenerative diseases such as ALS (can serve as an early marker for some SOD mutant mice models as reactive astrogliosis is observed at 5 weeks while motor neuron loss is seen only at 15 weeks),Alzheimers and Parkinsons Disease(astrocytes can secrete MPTP like toxins. Microglia could be causative for astrogliosis).
Dr Sajish Chandran successfully defended his PhD work entitled: "Evaluation of autonomic functions and neuroimaging studies in children prenatally exposed to alcohol"
Guide: Dr TN Sathyaprabha (Additional Professor, Neurophysiology)
Co-Guide: Dr Pratima Murthy (Professor, Psychiatry)
Examiner: Dr KK Deepak, (Professor, Physiology, AIIMS, Delhi)
Suwarna Chakraborty (1st year PhD Scholar) presented her seminar on "Role of Cerebellum in Cognition".
After providing an anatomical overview, she reviewed the well known motor functions of the different deep nuclei. The dentate nucleus (cerebro-cerebellum), which is the largest and connected to the cerebrum, works as a comparator that generates an error signal and provides planning and timing information.The other nuclei - Fastigious, emboliform and globase (spino-cerebellum) - have output to the spinal tracts and is involved in fine movements. The vestibulo cerebellum is involved in posture maintenance and eye movements.
The Mossy fibers (from the vestibular nuclei) and the climbing fibres (from the inferior olive) both provide input the Purkinje fibres. The former provide input on the context and the latter forms the error signal. Interestingly, Long Term Depression (LTD) which forms the memory element of the cerebellar motor learning, happens when both these fibre tracts are simultaneously active. If only one these fibre pathways are active, LTP (Long Term Potentiation) ensues. Therefore the cerebral cortex and the cerebellum have different mechanisms for LTP and LTD.
Suwarna then reviewed a number of studies evaluating cognitive functions and cerebellum. These included attention, working memory and spatial memory in various animal models (eg: pcd - purkinje cell degeneration model).
Dr Harsha HN successfully defended his PhD work entitled "Neurobiology of Auditory Verbal Hallucinations in Schizophrenia - An integrated fMRI, EEG and Genomics based approach".
Guide: Dr Bindu M Kutty (Prof, Neurophysiology)
Co-Guides: Dr Sanjeev Jain (Prof, Psychiatry) and Dr John P John (Additional Prof, Psychiatry)
Examiner: Dr K Srinivasan (Dean, St John's Research Institute and Professor of Psychiatry)
Kumari Anshu Jha (2nd year PhD scholar) presented her seminar on "Interneuron dysfunction in neuropsychiatric disorders". She focused on GABAergic dysfunction in Schizophrenia and Autism.
Anshu gave an overview of Interneuron functions (feedback & feedforward inhibition, network oscillations and synchrony, modulation of excitability, integration and cortical development and plasticity) and then highlighted the complexity of internuron types (classified based on morphological, molecular, electrophysiological properties - eg Markram 2004).
She then discussed the role of GABAergic neurons in the pathophysiology of Schizophrenia and then Autism from post-mortem studies and animal models (gene knockouts) while showing that GABA impairment seems to be present in a wide variety of neuropsychiatric disorders. She then went through the mechanisms through which these interneurons modulate network oscillations via electrical gap junctions and neurochemical modulations amongst the interneurons (for example Parvalbumin expressing basket cells impact gamma oscillations while somatostatin expressing interneurons impact beta oscillations).
Considering that the type of impairment is similar for schizophrenia and autism, the timing of the impairment seems to be a differentiator between these two disorders. Autism is seen in early childhood (diagnosed around 3 years of age when neuronal pruning is still ongoing) and the first onset of Schizophrenia happens in adolescence (when the neurons are fully formed but the myelination is still an ongoing process).