Center for Molecular Neurobiology Hamburg: Difference between revisions

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==Education==
==Education==


Training of graduate students and postdoctoral fellows is an integral part of the mission of the ZMNH. A '''Graduate Program in Molecular Biology and Neuroscience''' was established at the University-Hospital Hamburg Eppendorf in 1986 to promote in a multi-disciplinary approach the ability for scientific thinking and working. This Graduate Program presents molecular biology and neuroscience within a broader context of the basic sciences and biomedicine. Fundamental (basic) and clinical (applied) aspects are explored and are integrated with relevant areas of other disciplines. This course, which is organized by the ZMNH, is of particular value to those who plan a career in academic biomedical research or in a related industry.
Training of graduate students and postdoctoral fellows is an integral part of the mission of the ZMNH. A ''Graduate Program in Molecular Biology and Neuroscience'' was established at the University-Hospital Hamburg Eppendorf in 1986 to promote in a multi-disciplinary approach the ability for scientific thinking and working. This Graduate Program presents molecular biology and neuroscience within a broader context of the basic sciences and biomedicine. Fundamental (basic) and clinical (applied) aspects are explored and are integrated with relevant areas of other disciplines. This course, which is organized by the ZMNH, is of particular value to those who plan a career in academic biomedical research or in a related industry.

==Major discoveries==
Several proteins that are key to ''synaptic function'' were first cloned and characterized at the ZMNH, for example the presynaptic proteins Piccolo ([[PCLO]]) and Bassoon and the major organizer of the postsynaptic density, [[PSD-95]] (a.k.a. SAP90).<ref>{{cite journal|last1=Dieck|first1=S.|title=Bassoon, a Novel Zinc-finger CAG/Glutamine-repeat Protein Selectively Localized at the Active Zone of Presynaptic Nerve Terminals|journal=The Journal of Cell Biology|date=27 July 1998|volume=142|issue=2|pages=499–509|doi=10.1083/jcb.142.2.499}}</ref><ref>{{cite journal|last1=Kistner|first1=U|last2=Wenzel|first2=BM|last3=Veh|first3=RW|last4=Cases-Langhoff|first4=C|last5=Garner|first5=AM|last6=Appeltauer|first6=U|last7=Voss|first7=B|last8=Gundelfinger|first8=ED|last9=Garner|first9=CC|title=SAP90, a rat presynaptic protein related to the product of the Drosophila tumor suppressor gene dlg-A.|journal=The Journal of biological chemistry|date=5 March 1993|volume=268|issue=7|pages=4580-3|pmid=7680343}}</ref>
Synaptic activity controls the activity of certain genes, the so-called [[immediate early gene]]s. Arg3.1/[[Arc]], a prominent example of this gene family, was discovered at the ZMNH and found to have important functions in learning and memory.<ref>{{cite journal|last1=Link|first1=W.|last2=Konietzko|first2=U.|last3=Kauselmann|first3=G.|last4=Krug|first4=M.|last5=Schwanke|first5=B.|last6=Frey|first6=U.|last7=Kuhl|first7=D.|title=Somatodendritic expression of an immediate early gene is regulated by synaptic activity.|journal=Proceedings of the National Academy of Sciences|date=6 June 1995|volume=92|issue=12|pages=5734–5738|doi=10.1073/pnas.92.12.5734}}</ref><ref>{{cite journal|last1=Plath|first1=Niels|last2=Ohana|first2=Ora|last3=Dammermann|first3=Björn|last4=Errington|first4=Mick L.|last5=Schmitz|first5=Dietmar|last6=Gross|first6=Christina|last7=Mao|first7=Xiaosong|last8=Engelsberg|first8=Arne|last9=Mahlke|first9=Claudia|last10=Welzl|first10=Hans|title=Arc/Arg3.1 Is Essential for the Consolidation of Synaptic Plasticity and Memories|journal=Neuron|date=9 November 2006|volume=52|issue=3|pages=437–444|doi=10.1016/j.neuron.2006.08.024}}</ref>

An early focus of the center was understanding the structure and function of ''ion channels''. The famous 'ball-and-chain' mechanism of potassium channel inactivation was discovered at the ZMNH.<ref>{{cite journal|last1=Rettig|first1=Jens|last2=Heinemann|first2=Stefan H.|last3=Wunder|first3=Frank|last4=Lorra|first4=Christoph|last5=Parcej|first5=David N.|last6=Dolly|first6=J. O.|last7=Pongs|first7=Olaf|title=Inactivation properties of voltage-gated K+ channels altered by presence of β-subunit|journal=Nature|date=26 May 1994|volume=369|issue=6478|pages=289–294|doi=10.1038/369289a0}}</ref> A number of human diseases (hereditary forms of myotonia, osteopetrosis, retinal degeneration, kidney stone diseases, epilepsy, deafness) could be mapped to mutations in specific ion channels.<ref>{{cite journal|last1=Kubisch|first1=Christian|last2=Schroeder|first2=Björn C|last3=Friedrich|first3=Thomas|last4=Lütjohann|first4=Björn|last5=El-Amraoui|first5=Aziz|last6=Marlin|first6=Sandrine|last7=Petit|first7=Christine|last8=Jentsch|first8=Thomas J|title=KCNQ4, a Novel Potassium Channel Expressed in Sensory Outer Hair Cells, Is Mutated in Dominant Deafness|journal=Cell|date=February 1999|volume=96|issue=3|pages=437–446|doi=10.1016/S0092-8674(00)80556-5}}</ref><ref>{{cite journal|last1=Biervert|first1=C.|title=A Potassium Channel Mutation in Neonatal Human Epilepsy|journal=Science|date=16 January 1998|volume=279|issue=5349|pages=403–406|doi=10.1126/science.279.5349.403}}</ref><ref>{{cite journal|last1=Koch|first1=M.|last2=Steinmeyer|first2=K|last3=Lorenz|first3=C|last4=Ricker|first4=K|last5=Wolf|first5=F|last6=Otto|first6=M|last7=Zoll|first7=B|last8=Lehmann-Horn|first8=F|last9=Grzeschik|first9=K.|last10=Jentsch|first10=T.|title=The skeletal muscle chloride channel in dominant and recessive human myotonia|journal=Science|date=7 August 1992|volume=257|issue=5071|pages=797–800|doi=10.1126/science.1379744}}</ref><ref>{{cite journal|last1=Kornak|first1=Uwe|last2=Kasper|first2=Dagmar|last3=Bösl|first3=Michael R|last4=Kaiser|first4=Edelgard|last5=Schweizer|first5=Michaela|last6=Schulz|first6=Ansgar|last7=Friedrich|first7=Wilhelm|last8=Delling|first8=Günter|last9=Jentsch|first9=Thomas J|title=Loss of the ClC-7 Chloride Channel Leads to Osteopetrosis in Mice and Man|journal=Cell|date=January 2001|volume=104|issue=2|pages=205–215|doi=10.1016/S0092-8674(01)00206-9}}</ref> These fundamental insights allowed researchers to mimic important aspects of human diseases in genetically accurate animal models, a key step in the development of new drugs.<ref>{{cite journal|last1=Dahme|first1=Miriam|last2=Bartsch|first2=Udo|last3=Martini|first3=Rudolf|last4=Anliker|first4=Brigitte|last5=Schachner|first5=Melitta|last6=Mantei|first6=Ned|title=Disruption of the mouse L1 gene leads to malformations of the nervous system|journal=Nature Genetics|date=November 1997|volume=17|issue=3|pages=346–349|doi=10.1038/ng1197-346}}</ref>


==External links==
==External links==
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* [http://www.zmnh.uni-hamburg.de/blankenese_conferences/ Blankenese conferences], organized by the ZMNH
* [http://www.zmnh.uni-hamburg.de/blankenese_conferences/ Blankenese conferences], organized by the ZMNH
* [http://www.zmnh.uni-hamburg.de/teaching/asmb/asmb.html#eng_ver Graduate Studies in Molecular Biology] at the ZMNH
* [http://www.zmnh.uni-hamburg.de/teaching/asmb/asmb.html#eng_ver Graduate Studies in Molecular Biology] at the ZMNH

==References==


[[Category:Research institutes in Germany]]
[[Category:Research institutes in Germany]]

Revision as of 16:43, 18 December 2014

File:Center for Molecular Neurobiology Hamburg.jpg
ZMNH main entrance. Falkenried 94, 20251 Hamburg, Germany

The Center for Molecular Neurobiology Hamburg (ZMNH), founded in 1988, is an internationally recognized molecular neuroscience research center, part of the University Medical Center Hamburg-Eppendorf (UKE). Headed by Prof. Dr. Dietmar Kuhl, the ZMNH is currently home to 205 scientists and staff from 20 different countries (Dec. 2014).

Research

The focus of the ZMNH is basic research in neurobiology and neuroimmunology, combining molecular genetics with anatomical, biochemical and physiological approaches. The ZMNH is structured into five departments and several independent research groups.

Departments/Institutes

  • Molecular and Cellular Cognition (Prof. Dr. Dietmar Kuhl)
  • Molecular Neurogenetics (Prof. Dr. Matthias Kneussel)
  • Neuroimmunology and Multiple Sclerosis (Prof. Dr. Manuel A. Friese)
  • Structural Neurobiology (Prof. Dr. Dr. h.c. Michael Frotscher)
  • Synaptic Physiology (Prof. Dr. Thomas G. Oertner)

Independent Research Groups

  • Neuronal Development (Dr. Froylan Calderon de Anda)
  • Neuronal Translational Control (Dr. Kent Duncan)
  • Development and Maintenance of the Nervous System (Dr. Edgar Kramer)
  • Neuronal Patterning and Connectivity (Dr. Peter Soba)
  • Behavioral Biology Unit (Dr. Fabio Morellini)
  • Signal Transduction (Prof. Dr. Meliha Karsak)

Emeritus Group

  • Biosynthesis of Neural Structures (Prof. Dr. Melitta Schachner)

Guest Group

  • Developmental Neurophysiology (Prof. Dr. Ileana Hanganu-Opatz)

Research is supported by in-house facilities for Bioanalytics, Systems Biology, Morphology, Transgenic Animals, and Information Technology. The center has its own administration, machine shop, and library.

Education

Training of graduate students and postdoctoral fellows is an integral part of the mission of the ZMNH. A Graduate Program in Molecular Biology and Neuroscience was established at the University-Hospital Hamburg Eppendorf in 1986 to promote in a multi-disciplinary approach the ability for scientific thinking and working. This Graduate Program presents molecular biology and neuroscience within a broader context of the basic sciences and biomedicine. Fundamental (basic) and clinical (applied) aspects are explored and are integrated with relevant areas of other disciplines. This course, which is organized by the ZMNH, is of particular value to those who plan a career in academic biomedical research or in a related industry.

Major discoveries

Several proteins that are key to synaptic function were first cloned and characterized at the ZMNH, for example the presynaptic proteins Piccolo (PCLO) and Bassoon and the major organizer of the postsynaptic density, PSD-95 (a.k.a. SAP90).[1][2] Synaptic activity controls the activity of certain genes, the so-called immediate early genes. Arg3.1/Arc, a prominent example of this gene family, was discovered at the ZMNH and found to have important functions in learning and memory.[3][4]

An early focus of the center was understanding the structure and function of ion channels. The famous 'ball-and-chain' mechanism of potassium channel inactivation was discovered at the ZMNH.[5] A number of human diseases (hereditary forms of myotonia, osteopetrosis, retinal degeneration, kidney stone diseases, epilepsy, deafness) could be mapped to mutations in specific ion channels.[6][7][8][9] These fundamental insights allowed researchers to mimic important aspects of human diseases in genetically accurate animal models, a key step in the development of new drugs.[10]

External links

References

  1. ^ Dieck, S. (27 July 1998). "Bassoon, a Novel Zinc-finger CAG/Glutamine-repeat Protein Selectively Localized at the Active Zone of Presynaptic Nerve Terminals". The Journal of Cell Biology. 142 (2): 499–509. doi:10.1083/jcb.142.2.499.
  2. ^ Kistner, U; Wenzel, BM; Veh, RW; Cases-Langhoff, C; Garner, AM; Appeltauer, U; Voss, B; Gundelfinger, ED; Garner, CC (5 March 1993). "SAP90, a rat presynaptic protein related to the product of the Drosophila tumor suppressor gene dlg-A". The Journal of biological chemistry. 268 (7): 4580–3. PMID 7680343.
  3. ^ Link, W.; Konietzko, U.; Kauselmann, G.; Krug, M.; Schwanke, B.; Frey, U.; Kuhl, D. (6 June 1995). "Somatodendritic expression of an immediate early gene is regulated by synaptic activity". Proceedings of the National Academy of Sciences. 92 (12): 5734–5738. doi:10.1073/pnas.92.12.5734.
  4. ^ Plath, Niels; Ohana, Ora; Dammermann, Björn; Errington, Mick L.; Schmitz, Dietmar; Gross, Christina; Mao, Xiaosong; Engelsberg, Arne; Mahlke, Claudia; Welzl, Hans (9 November 2006). "Arc/Arg3.1 Is Essential for the Consolidation of Synaptic Plasticity and Memories". Neuron. 52 (3): 437–444. doi:10.1016/j.neuron.2006.08.024.
  5. ^ Rettig, Jens; Heinemann, Stefan H.; Wunder, Frank; Lorra, Christoph; Parcej, David N.; Dolly, J. O.; Pongs, Olaf (26 May 1994). "Inactivation properties of voltage-gated K+ channels altered by presence of β-subunit". Nature. 369 (6478): 289–294. doi:10.1038/369289a0.
  6. ^ Kubisch, Christian; Schroeder, Björn C; Friedrich, Thomas; Lütjohann, Björn; El-Amraoui, Aziz; Marlin, Sandrine; Petit, Christine; Jentsch, Thomas J (February 1999). "KCNQ4, a Novel Potassium Channel Expressed in Sensory Outer Hair Cells, Is Mutated in Dominant Deafness". Cell. 96 (3): 437–446. doi:10.1016/S0092-8674(00)80556-5.
  7. ^ Biervert, C. (16 January 1998). "A Potassium Channel Mutation in Neonatal Human Epilepsy". Science. 279 (5349): 403–406. doi:10.1126/science.279.5349.403.
  8. ^ Koch, M.; Steinmeyer, K; Lorenz, C; Ricker, K; Wolf, F; Otto, M; Zoll, B; Lehmann-Horn, F; Grzeschik, K.; Jentsch, T. (7 August 1992). "The skeletal muscle chloride channel in dominant and recessive human myotonia". Science. 257 (5071): 797–800. doi:10.1126/science.1379744.
  9. ^ Kornak, Uwe; Kasper, Dagmar; Bösl, Michael R; Kaiser, Edelgard; Schweizer, Michaela; Schulz, Ansgar; Friedrich, Wilhelm; Delling, Günter; Jentsch, Thomas J (January 2001). "Loss of the ClC-7 Chloride Channel Leads to Osteopetrosis in Mice and Man". Cell. 104 (2): 205–215. doi:10.1016/S0092-8674(01)00206-9.
  10. ^ Dahme, Miriam; Bartsch, Udo; Martini, Rudolf; Anliker, Brigitte; Schachner, Melitta; Mantei, Ned (November 1997). "Disruption of the mouse L1 gene leads to malformations of the nervous system". Nature Genetics. 17 (3): 346–349. doi:10.1038/ng1197-346.