Invited Symposium: Molecular Mechanisms of Ageing
Mason, CA (Center for Neurobiology & Behavior, College of Physicians & Surgeons of Columbia University, USA)
Morrison, ME (Center for Neurobiology & Behavior, College of Physicians & Surgeons of Columbia University, USA)
Neurotrophins such as BDNF cooperate with neuronal activity to modulate neuronal survival and dendritic differentiation. We studied whether TrkB signaling regulates development of dendrites and spines of Purkinje cells. BDNF treatment of purified Purkinje cells cultured alone did not elicit formation of mature dendrites or spines. In cocultures of granule and Purkinje cells, however, continuous treatment with BDNF over a 2 week postnatal period increased the density of Purkinje cell dendritic spines relative to control. The increase in spine density was blocked by adding TrkB-IgG fusion protein to the medium together with BDNF. Although BDNF did not change the morphology of dendritic spines, treatment with TrkB-IgG alone yielded spines with longer necks than those in control cultures. None of these treatments, however, altered the dendritic complexity of Purkinje cells. These analyses revealed a role for TrkB signaling in modulating spine development and showed that spine development can be uncoupled from dendritic outgrowth in this reductionist system of purified presynaptic and postsynaptic neurons.
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|Shimada, A; Mason, CA; Morrison, ME; (1998). TrkB Signaling Modulates Spine Density and Morphology Independent of Dendritic Complexity in Cultured Purkinje Cells. Presented at INABIS '98 - 5th Internet World Congress on Biomedical Sciences at McMaster University, Canada, Dec 7-16th. Invited Symposium. Available at URL http://www.mcmaster.ca/inabis98/higuchi/shimada0575/index.html|
|© 1998 Author(s) Hold Copyright|