SAVE THE DATE: 28 – 30 September 2021
INVITATION TO GENERAL ASSEMBLY We
cordially invite you to the next ANA General Assembly that will take
place ONLINE. Date: Wednesday September 23rd, 2020, 2:00 pm ANA members who want to join the event, please contact secretary@austrian-neuroscience.at for the respective zoom link. Agenda 1. Approval of the Minutes of the General Assembly from 26 September 2019 (pdf attached) 2. Report of the President (Francesco Ferraguti) 3. Report of the Secretary (René Seiger) 4. Report of the Treasurer (Petra Scholze) 5. Statement of the Auditors 6. Discharge of Treasurers 7. Discharge of Board 8. ANA Meeting 2021: Progress Report (Sébastien Couillard Despres & I. Sarto-Jackson) 9. Report of Young ANA (Bruno Benedetti) 10. Award Nomination: Pioneer in Austrian Neuroscience 11. ANA´s head office registration (Sébastien Couillard Despres & Isabella Sarto-Jackson) 12. Change of the Bylaws - Signing authority of ANA bank transfers (Petra Scholze) 13. Change of the Bylaws - The elected Vice President should automatically become President for the next term. In case he/she will not be available, both the President and the Vice President should be elected simultaneously. 14. Change of the Bylaws - Members for the Extended Board can be appointed for a maximum of 2 terms by the ANA Board. Extended Board members may be re-appointed only after a 2 terms interruption. 15. Proposals from Members (proposals must be conveyed in written form to the ANA secretary at least one week before the General Assembly) 16. Any other business
ANA is happy to announce that the following ANA members will receive a grant to participate in the FENS Virtual Forum 2020: Hugo Malagon (Medical University of Vienna)
FENS Virtual Forum 2020 & ANA Grants We are sure all of you know, that the Covid-19 pandemic prevents a “physical” FENS Forum this summer and that FENS has taken an enormous effort and challenge to convert the Forum into a virtual format, which will be online on the same dates: 11-15 July 2020. Many of you will wonder whether attending a virtual meeting is actually worth the time and money. The ANA Board believes that given the exceptional circumstances a virtual meeting is the best option available to keep promoting European Neuroscience at large. Hence, ANA strongly encourages its members to participate and contribute to the meeting. To promote this, ANA makes available grants for PhD students and young Postdocs (within 3 years from when they obtained their Doctoral degree), who are members of ANA, to cover up to 75% of the registration fee (calculated on the basis of the Student Member fee). (see details) Should you wish anyway to withdraw your registration and get reimbursed 100% of the fee, please be aware that you can do so only before the 22nd April 2020. For further information go to FENS 2020 Virtual Forum FAQ, Cancellation and Reimbursement (FENS Virtual Forum Q&A). With best wishes The ANA Board
FENS Forum 2020 Goes Virtual! Please follow updates on the FENS Forum Website
ANA 2019 Best Thesis Award: 2 winners ANA congratulates Stefanie Geisler and Anna Tröscher,
completed her thesis work under the supervision of Gerald Obermair, Department of Physiology, Medical University Innsbruck, Austria. A link to the Medical University of Innsbruck thesis repository will be set here as soon as all her thesis work has been published. Title: Redundant and specific functions of neuronal calcium channel α2δ isoforms in mutant mouse models and cultured neurons Abstract: The four auxiliary α2δ isoforms of voltage-gated calcium channelshave been implicated in synaptogenesis and neurological disorders. Yet, the molecular mechanisms by which individual isoforms exert synaptic functions in health and disease remainlargely elusive. This lack of mechanistic insight can be partly ascribed to the fact that many brain regions simultaneously express α2δ-1, α2δ-2 and α2δ-3. Here we show that neuronal α2δ isoforms act partially redundant, but have also highly specific functions. By generating and characterizing three distinct double knockout mouse models, we first demonstrate a general importance in survival and development. The augmented severity of the phenotype in double compared to single knockout mice further supports the idea of functional redundancy. Nevertheless, volumetric analysis of brain sections revealed a reduced size of distinct brain regions, suggesting specific roles of individual α2δ isoforms. Indeed, using primary neuronal cultures from embryonic mice we show that presynaptic overexpressionof the α2δ-2 isoform strongly increases clustering of postsynaptic GABAA-receptors (GABAAR) in GABAergic synapses. Strikingly, presynaptic α2δ-2 exerts the same effect in glutamatergic synapses, leading to an abnormal localization of GABAARs opposite glutamatergic nerve terminals. Employing super-resolution microscopy we further demonstrate that this mismatched synapse formation is caused by an aberrant wiring of glutamatergic presynaptic boutons with GABAergic postsynaptic positions. The property of α2δ-2 to induce mismatched synapses is independent of the prototypical cell-adhesion molecules α-neurexins. However, exclusion of a single alternatively spliced exon is essential for the trans-synaptic recruitment of GABAAR. Taken together, the findings presented in this thesis propose that α2δ isoforms regulate synaptic connectivity of glutamatergic and GABAergic neurons depending on exon usage. Our results thus provide a novel mechanistic explanation for how abnormal α2δ subunit expression can result in aberrant neuronal wiring associated with neurological disorders, including epilepsy and autism.
completed her thesis work under the supervision of Jan Bauer, Division of Neuroimmunology, CBR, Medical University of Vienna. Here you find her complete thesis. Title: Inflammation and Viruses in Epilepsy Abstract: Epilepsy is one of the most common neurological diseases but a third of patients do not respond to pharmacological treatment. Of those, many suffer from immune-mediated epilepsy, which can arise from the innate and adaptive immune system. Adaptive immune reactions can comprise of a T cell-or a humoral response. Depending on the immunological pathway activated and the brain area affected, the symptoms vary. Antibody-mediated encephalitis, such as anti-leucine-rich glioma-inactivated (LGI)-1 encephalitis, leads to limbic encephalitis, accompanied by memory disturbances, psychosis and seizures. T cell-mediated encephalitis, for example Rasmussen encephalitis (RE), causes seizures and severe brain atrophy, and hence cognitive defects. Many questions regarding immune-mediated epilepsies have not been answered yet and are difficult to address due to lack of tissue or its scarcity. Hence, we took advantage of a natural animal model, in which cats develop antibodies againstLGI1 and show symptoms similar to the human disease to analyze changes outside the hippocampus in LGI1-encephalitis. We could show that T cell infiltrates occur brain-wide and do not overlap with blood-brain-barrier leakage. Further a tight-junction protein is lost in the hippocampus and the amygdala, causing immunoglobulin leakage, leading to complement deposition on neurons and hence neurodegeneration. In addition, we established a method to perform whole-genome transcriptomic studies on minimal amounts of formalin-fixed paraffin-embedded tissue to identify innate and adaptive immune responses in RE, a prime model of T cell-mediated diseases. We were able to show that small microglia nodules precede the T cell influx, providing an inflammatory microenvironment characterized by endosomal Toll-like receptor (TLR) and inflammasome upregulation. With disease progression, T cells intermingle with the microglia nodules, where they attack and kill neurons. Neonatal microglia cultures showed similar expression profiles upon TLR3 stimulation to what was observed in RE, indicating a TLR induced inflammatory reaction. Taken together, we were able to explain human pathology underlying pathomechanisms leading to two different forms of drug-resistant epilepsy.
Jury for the 2019 Best Thesis Award: Sigismund Huck (ANA President); Christian Humpel (Loewi Award 2001); Johannes Berger (Loewi Award 2003); Harald Sitte (Loewi Award 2007).
You can now view the fantastic program of the FENS Forum in Glasgow (July 11-15, 2020). Please note that as ANA member you may submit travel grant applications to both FENS and ANA. For details please visit the Forum or our ANA Website, respectively.
!!! Please check information on FENS (Cajal) courses, Brain Conferences, and FENS Schools at "Upcoming Events "!!!
ANA honors Hans Winkler as Pioneer in Austrian Neuroscience
Hans Winkler graduated in Medicine in Innsbruck, did his D. Phil. with Herman Blaschko at the Department of Pharmacology, University of Oxford, and became Professor of Biochemical Pharmacology at the Leopold-Franzens University of Innsbruck in 1975. He succeeded Heribert Konzett in 1980 as head of the Department of Pharmacology. Hans Winkler collaborated for many years with David Smith (Oxford) and contributed as member of the editorial board from the beginning to “Neuroscience”, the IBRO journal founded by David Smith. Hans Winkler was a member of EMBO and of the DANA/EDAB alliance for the Brain. His oeuvre includes >250 publications with more than 10.000 citations.
Poster Prizes Oral Presentation Prizes
260 Participants attended the ANA/APHAR Meeting 2019! The meeting took place at the Center for Chemistry and Biomedicine (CCB) in Innsbruck and was a joint venture with the Austrian Pharmacological Society (APHAR). In addition, it was preceded by the final event of the FWF-funded Spezialforschungsbereich SFB-F44, which added a number of high-profile international speakers.
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At the occasion of the ANA/APHAR 2019 Meeting in Innsbruck, ANA President Sigismund Huck and the incoming ANA President Francesco Ferraguti honored Hans Winkler for his groundbreaking discoveries on peptidergic neurotransmission. The focus of his research were large dense-core vesicles, their content in neurosecretory proteins such as the chromogranins, and the biochemical characterization of the ATP-transporter on these vesicles.
