7. Conclusions and Outlook
The studies reviewed here have shown that the lack of a spine apparatus in synaptopodin-deficient mice is accompanied by changes in synaptic plasticity which are relevant for spatial learning. As pointed out at several places, further detailed analysis of synaptopodin-deficient mice is needed to better understand the role of synaptopodin in the formation and function of the spine apparatus and to determine to what extent compensatory changes due to the deletion of synaptopodin are involved. So far, we have established a role for synaptopodin in LTP at Schaffer collateral synapses in CA1. Numerous studies have shown that different mechanisms underlie LTP in CA3 which remains to be studied in synaptopodin-deficient mice. Along this line, we have not yet looked at long-term depression (LTD) in synaptopodin-deficient mice. LTD is a form of synaptic plasticity that is regularly observed in Purkinje cells while LTP can hardly be induced in these neurons. Wildtype Purkinje cells do not express synaptopodin and lack a spine apparatus. Can we change synaptic plasticity in these neurons by transfecting them with synaptopodin cDNA? Can transfection of hippocampal neurons from synaptopodin mutants rescue LTP and the formation of spine apparatuses? We are convinced that further analysis of synaptopodin-deficient mice will allow us to learn more about the function of an interesting protein and a characteristic organelle in dendritic spines of the cerebral cortex.
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Frotscher, M., Deller, T. (2005). Role of the Spine Apparatus in Synaptic Plasticity. In: Stanton, P.K., Bramham, C., Scharfman, H.E. (eds) Synaptic Plasticity and Transsynaptic Signaling. Springer, Boston, MA. https://doi.org/10.1007/0-387-25443-9_29
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