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Principle investigator: Detlef Balschun

The use of genetically engineered mice provides an elegant tool to explore the function of newly identified genes / proteins in their physiological context. However, when 'conventional' knock-out and transgenic mice are employed, the risk of an intrinsic compensation of the particular genetic change that may occur during development has to be considered. This serious concern and other important factors have been exhaustively discussed elsewhere (e.g. Wolfer and Lipp 2000, Exp Physiol. 2000 85:627-34; Gerlai 2001, Behav Brain Res. 2001 125:13-21; Wolfer et al. 2002, Trends Neurosci. 2002 25:336-40). Although the generation of strains with an inducible knock-out or transgene reduces this risk it is not completely eliminated.

During the last years we characterized long-term potentiation (LTP), long-term depression (LTD) and depotentiation (DP) in a number of knock-out strains with a deletion or reduction of genes that have been suggested to play a central role in the processes of induction and consolidation of synaptic plasticity and learning [e.g. ryanodine-receptor 3 (Balschun et al., 1999) , neurogranin (Pak et al., 2000) {Huang, Huang, et al. 2004 5296 /id} , Arg3.1, PSD-95, CREB {Gass, Wolfer, et al. 1998 20 /id} {Balschun, Wolfer, et al. 2003 1004 /id} ]. For others such as the protooncogene Mas a crucial role in synaptic plasticity could be elucidated (Walther et al., 1998) that has been repeatedly confirmed since then.

We will proceed in testing genetically-engineered mice for changes in hippocampal synaptic plasticity (LTP, LTD, DP). Mice strains that are of high-scientific interest for the field will be investigated as academic collaboration. Because of the limited resources of the 'public sector' of our group, other mice strains can only be tested as contract research at a fair rate in the FAN gGmbH (LINK zu FAN-Homepage) .


 

References:
Balschun D, Wolfer DP, Bertocchini F, Barone V, Conti A, Zuschratter W, Missiaen L, Lipp HP, Frey JU, Sorrentino V (1999) Deletion of the ryanodine receptor type 3 (RyR3) impairs forms of synaptic plasticity and spatial learning. EMBO J 18: 5264-5273.
Balschun D, Wolfer DP, Gass P, Mantamadiotis T, Welzl H, Schutz G, Frey JU, Lipp HP (2003) Does cAMP response element-binding protein have a pivotal role in hippocampal synaptic plasticity and hippocampus-dependent memory? J Neurosci 23: 6304-6314.
Gass P, Wolfer DP, Balschun D, Rudolph D, Frey U, Lipp HP, Schutz G (1998) Deficits in memory tasks of mice with CREB mutations depend on gene dosage. Learn Mem 5: 274-288.
Huang KP, Huang FL, Jager T, Li J, Reymann KG, Balschun D (2004) Neurogranin/RC3 enhances long-term potentiation and learning by promoting calcium-mediated signaling. J Neurosci 24: 10660-10669.
Pak JH, Huang FL, Li J, Balschun D, Reymann KG, Chiang C, Westphal H, Huang KP (2000) Involvement of neurogranin in the modulation of calcium/calmodulin-dependent protein kinase II, synaptic plasticity, and spatial learning: a study with knockout mice. Proc Natl Acad Sci U S A 97: 11232-11237.
Walther T, Balschun D, Voigt JP, Fink H, Zuschratter W, Birchmeier C, Ganten D, Bader M (1998) Sustained long term potentiation and anxiety in mice lacking the Mas protooncogene. J Biol Chem 273: 11867-11873.

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