The Cortex Club connects researchers at the University of Oxford with world-leading neuroscientists through a unique educational forum dealing with cutting-edge topics and significant challenges in neuroscience. Our events range from small intense debates with up-and-coming scientists to large discussion sessions led by internationally prominent speakers, followed by the opportunity to ask them questions over drinks.
We are excited to announce our final event of the year!
On Wednesday 11th December at 5 pm in the Sherrington Library,
in collaboration with the Centre for Neural Circuits and Behaviour (CNCB), we are hosting a panel discussion on Sleep: Features and Functions with:
Prof. Amita Sehgal, from the University of Pennsylvania;
Prof. Penelope Lewis, from the Cardiff University;
Dr. Jason Rihel, from University College London;
Prof. Stuart Peirson, Group Leader in the Sleep & Circadian Neuroscience Institute, University of Oxford.
The Panel discussion will be followed by a Christmas-themed drinks reception, then everybody is welcome to join us to a pub for dinner with the speakers.
If you would like to join us for after-talk pub with the speakers, please sign up at: https://forms.gle/De2Ddto9nQnvg9qc9
On Friday 6th December, we are co-hosting with DPAG a Q&A lunch after-talk at 2pm in the Sherrington Library with Professor Guillermina Lopez-Bendito.
If you would like to join us for free lunch, please sign up at: https://forms.gle/D3BGrRw5zZNgRWge6
The talk, instead, will be held at 1 pm in the Large Lecture Theatre, Sherrington Building, Off Parks Road, OX1 3PT.
Title: Clonal Lineage determines the direct conversion of thalamic astrocytes into subtype-specific thalamocortical neurons
Forced expression of defined transcription factors leads to the direct conversion of various cell types into induced neurons (iNs). Specifically, successful reprogramming of resident brain astrocytes in vitro as well as in vivo represents a great advantage for the generation of neurons and derived circuits. However, whether astrocytes from distinct brain regions might show a reprogramming specificity towards a unique iN type remains largely unknown. Here, we use direct reprogramming of thalamic astrocytes by Neurog2 to generate specific excitatory sensory-modality thalamocortical neurons. Moreover, we show that the origin, but not the environment of the astrocytes determines the fate of the iNs after direct reprogramming. Indeed, clonal analysis in the thalamus shows that astrocytes from the distinct thalamic nuclei are clonally related determining the specificity of the iNs generated from those astrocytes. We also found that the potential of the same transcription factor to reprogram nuclei-specific thalamic astrocytes into precise subsets of thalamocortical neurons depends on particular epigenetic modifications. In sum, our study provides novel insights into the mechanisms that control the specification of thalamic neurons and importantly those that are required for direct programming of sensory neurons. Generation of specific sensory brain circuits might be an approach for future rehabilitation strategies.
On Thursday, 28th November at 4 pm in the Sherrington Room, we are excited to welcome Dr. Daniel Del Toro, from Max Planck Institute of Neurobiology, who will be giving a talk entitled ”Synaptic proteins guide cortical migration and influence cortex folding’.
All Welcome! If you would like to join us for after-talk pub with the speaker, please sign up at: https://forms.gle/CprmcTazTWQcxukH9
A fundamental question in neuroscience is which mechanisms drive folding of the cerebral cortex. One of the most obvious feature of mammalian brain evolution is the expansion of the cortex, which is generally accompanied by substantial folding of the cortical surface into valleys (gyri) and ridges (sulci). This process represents a fascinating evolutionary step that highly impacts on neuronal network and cognitive capacity of large mammals. During development two important events shape the morphology of the cortex, the amplification of basal progenitors generating neurons, and the migration of the latter leading to the layered structure of the cortex. While amplification of basal progenitor cells represents a key event to induce gyration of the mammalian cortex, our knowledge on how neuronal migration and its lateral dispersion impacts cortex folding is scarce. Indeed, several studies have shown that migrating neurons in folded cortices have increased cellular dynamics, exploratory behaviour and lateral dispersion than those in the rodent brain with smooth surface, but the nature of this mechanism remains unknown. The problem can be broken down in several aspects: (i) genes: which molecules modulate lateral dispersion of migrating neurons, (ii) function: how lateral dispersion of neurons controls cortex folding. In this talk I will report on our research in understanding the relative contribution of cortical migration to folding of the mammalian cerebral cortex. I will exemplify this process by talking about how synaptic adhesion receptors are (re-)used during early cortical development to guide cortical migration and describe techniques to analyze intercellular adhesive and repulsive interactions.
On Friday, Nov 22, we have a special lecture as part of the Joint Oxford-Berlin Neuroscience meeting: www.dpag.ox.ac.uk/events/oxford-berlin-symposium.
Join us for a talk given by Professor Matthew Larkum on ‘Coupling the state and contents of consciousness’.
We are excited to welcome Professor Marcello Massimini, from the University of Milan, on Tuesday 19th November, at 4 pm in the Small Lecture Theatre, Sherrington Building, Off Parks Road, OX1 3PT.
Professor Massimini will be giving a talk on ‘OFF-periods, causality and complexity in cortical networks during loss and recovery of Consciousness‘.
All Welcome! If you would like to attend the talk, please sign up at: https://cortex-club-massimini.eventbrite.co.uk .
Theoretical neuroscience suggest that consciousness depends on the ability of neural elements to engage in complex activity patterns that are, at once, distributed within a system of interacting cortical areas (integrated) and differentiated in space and time (information-rich) (i.e. brain complexity). Based on this principle, we have been developing and testing a theory-driven empirical method to assess brain complexity based on a combination of transcranial magnetic stimulation (TMS) and electroencephalography (EEG). Overall, the estimation of brain complexity provides a reliable measuring scale along the unconsciousness/consciousness spectrum and allows a robust assessment of unresponsive individuals (such as locked-in, minimally conscious and vegetative state patients) whose level of consciousness cannot be assessed behaviorally.
Starting from the experimental evidence of a link between consciousness and complexity, we moved on to explore the mechanisms by which brain complexity collapses and recovers in the human brain. Specifically, we wanted to test the hypothesis that neuronal bistability – the intrinsic tendency of cortical neurons to fall into a silent OFF-period after an initial activation – may play an important role in impairing the brain’s capacity to engage in complex patterns of causal interactions not only during NREM sleep but also in anesthesia and in brain-injured patients. We address this question at multiple scales (macro, meso and micro) of investigation, by recording brain responses to direct cortical stimulations using (1) TMS/EEG, (2) intracranial electrical stimulation/recordings in neurosurgical patients as well as (3) in cortical slices. These measurements provide convergence evidence that bistability and neuronal OFF periods may play an important role in disrupting causality and in preventing the build-up of brain complexity. Since bistability is, in principle, a reversible dynamics, this finding may point to novel strategies to promote recovery of consciousness after brain injury.