She elaborated on important electrical properties of neuronal membrane that helps in neuronal signal transmission.There was good discussion on the capacitance, time constant and length constant property of the neuronal membrane.There was good discussion on the capacitance, time constant and length constant property of the neuronal membrane.
Kala P Nair (2nd year MPhil scholar) presented a seminar titled "Ionic basis of neuronal signalling".
She elaborated on important electrical properties of neuronal membrane that helps in neuronal signal transmission.There was good discussion on the capacitance, time constant and length constant property of the neuronal membrane.There was good discussion on the capacitance, time constant and length constant property of the neuronal membrane. Kumaresan (MPhil Scholar) reviewed the basics of Potassium channels in his seminar, covering the various approaches to classification, mode of action and also shared the deveresearch in this area.
Vrinda M (4 year PhD Scholar) presented the paper by Alvestad etal from Epilepsy Research 2013 entitled "Mislocalization of AQP4 precedes chronic seizures in the kainate model of temporal lobe epilepsy"
Summary It has been suggested that loss of the astrocytic water channel aquaporin-4 (AQP4) from perivascular endfeet in sclerotic hippocampi contributes to increased seizure propensity in human mesial temporal lobe epilepsy (MTLE). Whether this loss occurs prior to or as a consequence of epilepsy development remains to be resolved. In the present study, we investigated whether the expression and distribution of AQP4 was altered prior to (i.e., in the latent phase) or after the onset of chronic epileptic seizures (i.e., in the chronic phase) in the kainate (KA) model of MTLE. Immunogold electron microscopic analysis revealed that AQP4 density in adluminal endfoot membranes was reduced in KA treated rats already in the latent phase, while the AQP4 density in the abluminal endfoot membrane was stable or slightly increased. The decrease in adluminal AQP4 immunogold labeling was accompanied by a reduction in the density of AQP4’s anchoring protein alpha-syntrophin. The latent and chronic phases were associated with an upregulation of the M1 isoform of AQP4, as judged by semi-quantitative Western blot analysis. Taken together, the findings in this model suggest that a mislocalization of AQP4 — reflecting a loss of astrocyte polarization — is an integral part of the epileptogenic process. Maltesh K (1st year PhD Scholar) presented the paper by Warden et al from Nature 2012 entitled: "A prefrontal cortex–brainstem neuronal projection that controls response to behavioural challenge"
Abstract The prefrontal cortex (PFC) is thought to participate in high-level control of the generation of behaviours (including the decision to execute actions); indeed, imaging and lesion studies in human beings have revealed that PFC dysfunction can lead to either impulsive states with increased tendency to initiate action, or to amotivational states characterized by symptoms such as reduced activity, hopelessness and depressed mood. Considering the opposite valence of these two phenotypes as well as the broad complexity of other tasks attributed to PFC, we sought to elucidate the PFC circuitry that favours effortful behavioural responses to challenging situations. Here we develop and use a quantitative method for the continuous assessment and control of active response to a behavioural challenge, synchronized with single-unit electrophysiology and optogenetics in freely moving rats. In recording from the medial PFC (mPFC), we observed that many neurons were not simply movement-related in their spike-firing patterns but instead were selectively modulated from moment to moment, according to the animal’s decision to act in a challenging situation. Surprisingly, we next found that direct activation of principal neurons in the mPFC had no detectable causal effect on this behaviour. We tested whether this behaviour could be causally mediated by only a subclass of mPFC cells defined by specific downstream wiring. Indeed, by leveraging optogenetic projection-targeting to control cells with specific efferent wiring patterns, we found that selective activation of those mPFC cells projecting to the brainstem dorsal raphe nucleus (DRN), a serotonergic nucleus implicated in major depressive disorder, induced a profound, rapid and reversible effect on selection of the active behavioural state. These results may be of importance in understanding the neural circuitry underlying normal and pathological patterns of action selection and motivation in behaviour. Merlin PB (1st year MPhil Scholar) presented her first seminar on the "Structure and Function of Ion Channels".
Merlin discussed about the conductivity, selectivity and gating mechanisms of Ion channels, various types of ion channels based on function, different channel protein families related by structural similarity, channel agonists and antagonists and the developmental changes in ion channel properties. Nesin Mathew (Junior Research Fellow) presented her first seminar on the topic "Signalling at the Neuromuscular Junction".
She started with a historical perspective - the discovery of the first neurotransmitter by Otto Loewi. She went onto explain the details of the anatomical, electrophysiological and molecular basis of signalling at the neuromuscular junction sharing both classical studies and recent findings. She ended with a quick overview of the developmental aspects as well as associated diseases. A significant coverage of a vast topic in a comprehensive manner. Suresh Parmar (1st year MPhil Scholar) presented an in-depth seminar on Ion channels exploring the various types, conduction mechanisms, gene families, blockers etc. He managed to cover both breadth and depth in a well connected manner and the talk was appreciated.
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