DCN Symposium on Molecules to Behaviour

DCN Symposium on Molecules to Behaviour

7 December 2015 09:00 hrs. - 12:00 hrs.
Location see remarks
DCN Symposium on Molecules to Behaviour
07-12-2015 09:00:0007-12-2015 12:00:00Europe/AmsterdamDCN Symposium on Molecules to Behaviour Location see remarksRimlsrimls@radboudumc.nl

Remarks / more information:

Location: HG00.062 (Radboud University).



Developmental mechanisms that establish neuronal diversity in the dopaminergic system
Dr. Sandra Blaess, University of Bonn
Midbrain dopaminergic neurons (MbDNs) are essential for modulating important brain functions including reward behavior, voluntary movement and cognitive processes. MbDNs are diverse in their afferent and efferent connections, morphologies, molecular profiles, electrophysiologial properties and in vivo activity. In recent years progress has been made in unraveling how some of these distinct properties might congregate to define a functionally distinct MbDN subtype. Nevertheless, our understanding of cellular diversity in the dopaminergic system is still limited and we know little about the mechanisms that control the generation of diverse subtypes of MbDNs and their specific connections. We are using innovative genetic tools in the mouse to investigate to which extend MbDN diversity is generated at the progenitor stage, how transcription factors that are expressed in subsets of developing MbDNs influence MbDN subtype fate and segregate into discrete neuronal clusters.

Molecular underpinnings of signaling specificity in synaptic plasticity
Ass. Prof. Oliver Schlüter, University of Pittsburgh
Repetitive NMDA-type glutamate receptor activation in principal neurons causes long-lasting changes in synaptic efficacy, which are likely cellular correlates of learning and memory. These processes are typically expressed as changes in synaptic numbers of AMPA-type glutamate receptors. The identity of the signaling cascade from NMDA receptor activation to changes in AMPA receptor numbers remains unknown. We hypothesise that PSD-95 related signaling scaffolds coordinate these signaling events and link receptor signaling with specific signaling pathways and effectors, such as AMPA receptors and other proteins. We identified different forms of synaptic plasticity, which depend on specific paralogs of the PSD-95 protein family, enabling us to further dissect the underlying signaling pathways and identify the role of these forms of plasticity in animal behaviour.

Flies and mice to unravel molecular mechanisms of neurodegenerative diseases
Dr. Erik Stoerkebaum, Max Planck Institute for Molecular Medicine
Neurodegenerative disorders are incurable diseases characterized by degeneration of specific neuronal populations. The molecular mechanisms are poorly understood and, with few exceptions, no effective therapies are available. We use Drosophila and mouse genetics as a complementary approach to decipher the molecular pathogenesis of motor neurodegenerative disorders, as genetic screens in Drosophila allow for the identification of putative disease modifying genes. Identified genes are validated in mouse models, before evaluating whether these pathways are also implicated in human patients.

The neuroethology of a complex behavior: from molecules to circuits, behavior and evolution.
Assoc. Prof. Mark Alkema, University of Massachusetts Medical School
Complex behaviors are thought to arise through the sequential activity of synaptically connected neurons. However, it has been difficult to fully understand how the brain translates sensory information into a behavioral output. The complete defined neural connectivity of the nematode C. elegans makes it particularly suited to study how sensorimotor processing occurs in behavior. Using a combination forward genetics, optogenetics and calcium imaging we analyze how the nematode brain orchestrates the escape response: a compound motor sequence that allows the animal to move away from a threatening predators.

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