Lectures(Alphabetical Order)

Speaker: Yang Dan (Neuro-Brain SuperComputing Whorkshop 2012)

  • Position: University of California, Berkeley
  • Title: Visual processing and the effect of neuromodulation
  • Abstract:

    　I will first present our recent studies using optogenetic, electrophysiology, and imaging techniques to dissect the visual cortical microcircuit, addressing the functional roles and rule of connectivity of both excitatory and inhibitory neurons. If there is time, I will also discuss our studies on the effect of the basal forebrain cholinergic system on modulating visual cortical circuits.

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Speaker: Shelley Halpain (Neuro-Brain SuperComputing Whorkshop 2012)

  • Position: University of California, San Diego
  • Title: 　 　Cytoskeletal mechanisms in neural circuit development & plasticity
  • Abstract:

    Structure and function are intimately related at all levels of biology. This holds particularly true for the the billions of cells, neurites, and synaptic connections that comprise the mammalian nervous system. Throughout development, these elements of the nervous system are over-produced, then scaled back through specific mechanisms that shape the ultimate wiring of the brain. Interestingly, the destabilization and removal of connections at the proper time and location is of equal importance to the initiation of connections. To support formation of neural connections, neurons must reorganize their subcellular structure in response to extracellular cues (for example, guidance cues for axonogenesis, activity cues for synaptogenesis). Our laboratory uses quantitative fluorescence microscopy and time-lapse imaging to study neurite formation, synapse development, and synapse loss in mammalian neurons. We focus on cytoskeletal mechanisms that transduce extracellular cues into morphological changes for the neuron. This talk will address specific molecular mechanisms that control the neuronal cytoskeleton in the context of development and synaptic plasticity. Evidence for the coordination of actin and microtubule function during early neurite formation will be presented. In addition, the role of actin cytoskeletal rearrangement in dendritic spines will be discussed in the context of both synaptic plasticity and neurodegenerative disease.

    　
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Speaker: Yuji Ikegaya

  • Position: The University of Tokyo
  • Title: Mesoscopic views of neuronal network activity
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Speaker: Kozo Kaibuchi

  • Position: Nagoya University
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Speaker: Arvind Kumar (Neuro-Brain SuperComputing Whorkshop 2012)

  • Position: University of Freiburg
  • Title: Dynamics and functional consequences of some inhibitory sub-cortical networks
  • Abstract:

    Part I: Computational mechanisms underlying formation of fear and extinction memories

    Classical fear conditioning is one of the most powerful models to study the neuronal mechanism underlying associative learning in the brain. Studies over the last decades have identified the amygdaloid complex as a key brain structure involved in both fear conditioning and extinction. The amygdaloid complex consists of several anatomically and functionally distinct subnetworks. The basolateral complex (BLA), which is subdivided in to the lateral (LA), and basal (BA) nuclei, is a network of both excitatory and inhibitory neurons similar to the neocortex. By contrast, the central amygdaloid complex (CEA), which can be divided in to the lateral (CEl), and medial (CEm) sub-networks, is an inhibitory network similar to the striatopallidal structure in the basal ganglia.

    How this serial cascade of neocortical and striatal like networks processes information is poorly understood despite the recent availability of in vivo data about average firing rates in various subnetworks of the amygdaloid complex.

    In my talk I will review a few key experimental observations about fear conditioning and extinction. Next, I will discuss computational models of lateral amygdala, basolateral amygdala and central amygdala. These reduced models of specific subnetworks provide important insights about the role of each network in the acquisition and extinction of fear memories. For instance, the model of the BLA suggests that extinction is masking the old fear memories by new memories. Similarly, the model of central amygdala reveals highly non-linear interactions between the lateral and medial subnetworks. Finally, I will discuss predictions of these various models and how they form the basis for computational models of brain disorders such as post-traumatic stress disorder and anxiety.

    Part II: Origin of oscillations in the basal ganglia: Implications for Parkinson's disease and action-selection

    The basal ganglia (BG) plays a critical role in multitude of cognitive and motor tasks. At the network, the BG is anatomically and functionally subdivided in to three inhibitory subnetworks, viz. the striatum, the globus pallidus external (GPe) and the globus pallidus internal (GPi). Striatum is the main input stage of the BG and it receives massive convergent and divergent projection of multiple brain regions. In addition, the GPe receives excitatory inputs from the sub-thalamic nucleus (STN). These sub-networks form three dominant pathways of the BG: direct pathway (involving striatum and GPi), indirect pathway (involving straiten, GPe and GPi) and hyper-direct pathway (STN, GPe, and GPi). These pathways form multiple excitatory-inhibitory loops that render the BG prone to pathological synchrony and oscillation which is thought to underly multiple cognitive and motor deficits observed in Parkinson's disease.

    In my talk using both simple firing rate based models as well as large network simulation, I will describe various mechanisms that can generate oscillations and discuss their biological plausibility. Specifically, I will discuss the role of the statistics of the striatal activity in the control and generation of oscillations and show that increase in striatal correlations and/or firing rates can unleash the oscillations in the BG, similar to that observed in the PD. Based on this observation, I will propose a unified explanation for different phenomena: absence of oscillation in the healthy state of the basal ganglia, oscillations in dopamine-depleted state and quenching of oscillations under deep-brain-stimulation (DBS). Finally, properties of the response transients in the BG also allow us to account for both motor impairment in PD patients and for reduced response inhibition in DBS implanted patients.

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Speaker: Hitoshi Okamoto

  • Position: RIKEN Brain Science Institute
  • Title: The roles of the habenula in aversive learning and gain of self-confidence in aggressive behavior
  • Abstract:

    The habenula (Hb) is an evolutionarily conserved diencephalic structure that acts as a relay nucleus connecting the limbic forebrain with the brain stem monoaminergic systems. In mammals, the Hb is subdivided into medial and lateral regions (MHb and LHb, respectively). We recently discovered that the dorsal and ventral Hb (dHb and vHb) of zebrafish correspond respectively to the MHb and LHb of mammals.

    In mammals, the LHb is activated by receiving the unpredictable aversive stimuli, and represses the activity of dopaminergic and serotonergic neurons. The functions of the MHb in mammals have long remained ambiguous. Recently, we demonstrated in zebrafish that the lateral subnuclei of the dorsal habenula (dHbL) are asymmetrically connected with the dorsal and intermediate parts of the interpeduncular nucleus (d/iIPN). This pathway further projects to the region containing the equivalents of the dorsal raphe, the periaqueductal gray, and the dorsal tegmental nuclei. Specific silencing of the dHbL-d/iIPN pathway rendered animals extraordinarily prone to freeze in response to conditioned fear stimuli, while the control fish showed only flight behaviors, implicating this pathway in experience-dependent reevaluation of danger during the fear conditioning trials. In this seminar, I will discuss how this capacity is utilized in the fish fight for determination of a winner and a loser.

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