Department of Neuroscience, University of Copenhagen (Rath group)
“Circadian oscillators of the cerebral cortex and cerebellum: evidence of roles and regulation from studies in rodent models”
We have investigated the physiological and molecular effects of genetic disruptions in the molecular clock in the cerebral cortex and the cerebellum, respectively. Furthermore, a possible hormonal signaling pathway from the central clock in the suprachiasmaticus nucleus to the circadian oscillators in the cerebral cortex and cerebellum is evaluated using programmable micropumps with corticosterone infused in a rhythm mimicking normal circadian fluctuations.
Andreas Toft Sørensen
Department of Neuroscience, University of Copenhagen (Gether group)
“A viral genetic platform for targeting multivalency in pain disorders”
In this talk, I will describe the concept, application, and development of a novel gene encoding platform, which allows for posttranslational assembly of multivalent recombinant peptides of clinical relevance, while harnessing on the cellular precision and intracellular delivery of AAV gene therapy. This AAV approach, if delivered intrathecally into the spinal dorsal horn, can completely reverse neuropathic pain in the spared nerve injury (SNI) model, hereby demonstrating an unconventional strategy of treating diseases involving glutamatergic dysfunction.
Department of Neuroscience, University of Copenhagen (Kiehn Group)
”Nimodipine prevents the development of spasticity after spinal cord injury”
Abstract: Spasticity, one of the most frequent comorbidities of spinal cord injury (SCI), has been show to disrupt motor recovery and quality of life. Despite major progress in neurorehabilitative and pharmacological approaches, no curative treatment for spasticity exists. Here, we show in a mouse model of chronic SCI that treatment with nimodipine – an FDA-approved L-type calcium channel blocker – starting in the acute phase of SCI completely prevents the development of spasticity. This aberrant muscle activity is permanently blocked even after termination of the treatment. Constitutive and conditional silencing of CaV 1.3 channels in different neuronal populations shows that preventive effect of nimodipine on spasticity after SCI is mediated by the neuronal CaV 1.3 channels. This study identifies a potentially curative treatment protocol with a specific target for the prevention of spasticity after SCI.
Followed by BEER and CHIPS