Q&A: Associate Prof Holly Bridge

Understanding the pathways underlying residual visual function after damage to primary visual cortex

Friday 1 February, 1pm at the Large Lecture Theatre, Sherrington Building, Oxford

 

 

The Cortex Club is delighted to present Associate Prof Holly Bridge from the Nuffield Department of Clinical Neuroscience, Oxford, who, as part of the DPAG Head of the Department seminar series, will be talking to us about her work on residual function after loss of vision.  Please join us on February 1st at the Large Lecture Theatre, located in the Sherrington Building of the Department of Physiology, Anatomy and Genetics.

We are hosting a Q&A session after the talk from 2.00 to 3.00 in the Cardiac Seminar Room. We warmly invite in particular students and postdocs to join us. Sandwiches provided. Please sign up at: https://goo.gl/forms/9MsoDV44W0OBbmIa2

 

 

Abstract

Damage to the primary visual cortex leads to loss of the visual field contralateral to the damaged cortex. However, in spite of this loss, some patients are still able to detect visual information about stimuli presented within their blind field. A growing area of research aims to exploit this residual visual function to try to improve visual performance through rehabilitation programmes stimulating the blind field. However, to optimise such programmes it is important to understand the pathways through which this information is conveyed. Here I will present a series of magnetic resonance imaging studies in which we attempted to elucidate these pathways in a group of hemianopic patients. Firstly I will explain how our functional MRI studies use the specific pattern of response to visual stimulation in different visual areas to uncover candidate pathways. I will use diffusion-weighted data to provide support for a pathway between the lateral geniculate nucleus and motion area MT that is consistently intact only in patients showing blindsight abilities. Finally, I will present our most recent data in which we find further support for this pathway using functional connectivity analysis.

Q&A: Prof Claus Hilgetag

An architectonic type principle integrates cerebral cortical architecture and connectivity

Friday 25 January, 1pm at the Large Lecture Theatre, Sherrington Building, Oxford

 

The Cortex Club is excited to presents Prof Claus Hilgetag from the Institute of Computational Neuroscience, UKE Hamburg, who, as part of the DPAG Head of the Department seminar series,  will be talking to us about his work on cortico-cortical connections to derive general principles of neuronal wiring in the cortex. Please join us on January April 14th at the Large Lecture Theatre, located in the Sherrington Building of the Department of Physiology, Anatomy and Genetics.

 

 

We are hosting a Q&A session after the talk from 2.00 to 3.00 in the Sherrington Library. We warmly invite in particular students and postdocs to join us. Sandwiches provided. Please sign up at at: https://goo.gl/forms/9OGq47ACcVgTvvzE2

 

 

Abstract

The connections that link neurons within as well as between cerebral cortical areas form a multi-scale structural network for communication in the brain. Which principles underlie the organisation of this complex network? We addressed this question by systematically investigating the relation of essential features of cortico-cortical connections, such as their presence or absence as well as patterns of laminar projection origins and terminations, to fundamental structural parameters of cortical areas, such as their distance, similarity in cortical cytoarchitecture as defined by cortical lamination or neuronal density, and similarity in further macroscopic and microscopic morphological features. These systematic analyses demonstrate the presence of an architectural type
principle. Across different species (mouse, cat, macaque monkey and human) and different cortices, the essential features of cortico-cortical connections vary consistently and strongly with the cytoarchitectonic similarity of cortical areas. By contrast, such relations were not found as consistently in multivariate analyses for distance, similarity
of cortical thickness or cellular morphological features. The presence of the architectonic type principle across mammalian brains allows direct cross-species predictions of the existence and laminar patterns of projections, including for the human brain, where such data are not directly available experimentally. Moreover, intrinsic brain architecture as characterised by architectural type and neural density also accounts for cellular neuronal features, such as cell size or shape. Thus, these findings illuminate a general principle of neural wiring and integrate cortical connectivity and architecture across scales of organisation, with implications for models of cortical physiology as well as developmental mechanisms.

 

Seminar: Prof Gero Miesenboeck

The Somnostat: Neuronal Machinery for Balancing Sleep Need and Sleep

Thursday 17 January, 4.15pm at the Large Lecture Theatre, Le Gros Clark Building, Oxford

 

 

The Cortex Club is delighted to start this year’s seminar series with Prof Gero Miesenboeck, Waynflete Professor at the CNCB Oxford, who will be talking to us about his research on the need for sleep. Please join us on January 17th at the Large Lecture Theatre, located in the Le Gros Clark Building of the Department of Physiology, Anatomy and Genetics.

 

If you would like to join us at the pub after the talk, please sign up at https://goo.gl/forms/AYwFmNuYcdpYGByD3 .

 

Abstract

Sleep is vital and universal, but its biological function remains unknown. We seek to understand why we need to sleep by studying how the brain responds to sleep loss. Our studies in Drosophila have pinpointed neurons whose sleep-inducing activity switches on as sleep deficits accrue, revealed how this activity switch works, and furnished a molecular interpretation of sleep pressure, its accumulation, and its discharge.

Seminar: Giulio Tononi

Sleep: A Window on ConsciousnessCentre for Neural Circuits and Behaviour at the University of Oxford

Tuesday 11 December, 12pm at the Oxford Martin School, Old Indian Institute, Oxford

 

The Cortex Club is delighted to co-host, together with the CNCB, Prof Giulio Tononi from the University of Wisconsin-Madison, who will be talking to us about his research on the role of sleep on consciousness. Please join us on December 11th at the Oxford Martin School, located in the Old Indian Institute at 34 Broad Street, Oxford.

 

For further information please contact Fiona Woods (fiona.woods – at – cncb.ox.ac.uk).

 

 

Abstract

How does consciousness come about, and how can the brain create a world even when it is disconnected from the environment? Consciousness never fades when we are awake. However, when awakened from sleep, we sometimes recall dreams and sometimes recall no experiences. Traditionally, dreaming has been identified with rapid eye-movement (REM) sleep, characterized by wake-like, globally ‘activated’, high-frequency EEG activity. However, dreaming also occurs in non-REM (NREM) sleep, characterized by prominent low-frequency activity. Recent work using no-task, within-state paradigms has identified a ‘posterior hot zone’ where the EEG must be activated for subjects to experience dreams. Localized, content-specific activations occur depending on whether one dreams of faces, places, movement, and speech. These findings highlight the likely neural substrate of our own experiences and suggest some of the necessary and sufficient conditions for consciousness.

Seminar: Prof. Chiara Cirelli

The price of being awake and the function of sleep: synaptic homeostasisCentre for Neural Circuits and Behaviour at the University of Oxford

Monday 10 December, 4pm at the Large Lecture Theatre, DPAG/Le Gros Clark Bldg

 

The Cortex Club is delighted to co-host, together with the CNCB, Prof Chiara Cirelli from the University of Wisconsin-Madison, who will be talking to us about her research on synaptic homeostastis during sleep. Please join us on December 10th at the Large Lecture Theatre, located in the Le Gros Clark Building of the Department of Physiology, Anatomy and Genetics.

Prof. Chiara Cirelli has kindly agreed to meet students and staff individually. If you would like to arrange a meeting please contact Fiona Woods (fiona.woods – at – cncb.ox.ac.uk).

 

To join us in the pub after the talk – where we’ll be joined by both Prof Cirelli and Prof Tononi – please register at https://goo.gl/forms/yxneVL15Nxs3YIDG3

 

Abstract
Sleep is universal, tightly regulated, and many cognitive functions are impaired if we do not sleep. But
why? Any hypothesis about the essential function of sleep must take into account that when asleep we
are essentially offline: sensory disconnection must be crucial for whatever function sleep serves. If not,
natural selection would likely have found a way to perform the same function while awake, avoiding
the danger of being unable to monitor the environment.

Over the past 20 years, we have developed and tested a comprehensive hypothesis about the core
function of sleep: The Synaptic Homeostasis Hypothesis (SHY). SHY states that sleep is the price we pay
for brain plasticity. During wakefulness the excitatory synapses that allow neurons to communicate
with each other undergo net potentiation as a result of learning, an ongoing process that happens all the
time while we are awake, constantly adapting to an ever-changing environment. The plasticity of the
brain is essential for survival but is also a costly process, because stronger synapses increase the
demand for energy and cellular supplies, lead to decreases in signal-to-noise ratios, and saturate the
ability to learn. According to SHY, the renormalization of synaptic strength should mainly occur
during sleep when the brain is disconnected from the environment and neural circuits can be broadly
reactivated off-line to undergo a systematic and yet specific synaptic down-selection. This
renormalization favors memory consolidation and the integration of new with old memories, and
eliminates the synapses that contribute more to the “noise” than to the “signal.” Just as crucially,
synaptic renormalization during sleep restores the homeostasis of energy and cellular supplies,
including many proteins and lipids that are part of the synapses, with beneficial effects at both the
systems and cellular level.

I will discuss the rationale underlying this hypothesis and summarize electrophysiological, molecular
and ultrastructural studies in flies, rodents and humans that confirmed SHY’s main predictions,
including the recent observation, obtained using serial block face scanning electron microscopy, that
most synapses in mouse primary motor and sensory cortices grow after wake and shrink after sleep. I
will then present unpublished ultrastructural data obtained in the hippocampus and in the cortex of
mouse pups. Finally, I will examine recent studies by other groups showing the causal role of cortical
slow waves and hippocampal ripples in sleep-dependent synaptic down-selection, and some of the
molecular mechanisms that can mediate this process.