title: CRMP5 (collapsin response mediator protein 5) regulates dendritic development and synaptic plasticity in the cerebellar Purkinje cells.
abstract: Collapsin response mediator protein 5 (CRMP5) is one of the CRMP members that expresses abundantly in the developing brain. To examine the in vivo function of CRMP5, we generated crmp5-deficient (crmp5(-/-)) mice. Anti-calbindin immunofluorescence studies of crmp5(-/-) mice revealed aberrant dendrite morphology; specifically, a decrease in the size of soma and diameter of primary dendrite of the cerebellar Purkinje cells at postnatal day 21 (P21) and P28, but not at P14. Coincidentally, CRMP5 is detected in Purkinje cells at P21 and P28 from crmp5(+/-) mice. In cerebellar slices of crmp5(-/-) mice, the induction of long-term depression of excitatory synaptic transmission between parallel fibers and Purkinje cells was deficient. Given that brain-derived neurotrophic factor (BDNF) plays major roles in dendritic development, we tried to elucidate the possible roles of CRMP5 in BDNF signaling. The effect of BDNF to induce dendritic branching was markedly attenuated in cultured crmp5(-/-) neurons. Furthermore, CRMP5 was tyrosine phosphorylated when coexpressed with neurotrophic tyrosine kinase receptor type 2 (TrkB), a receptor for BDNF, in HEK293T cells. These findings suggest that CRMP5 is involved in the development, maintenance and synaptic plasticity of Purkinje cells.
authors.affiliation: Department of Molecular Pharmacology and Neurobiology, Yokohama City University Graduate School of Medicine, Yokohama 236-0004, Japan.
authors.forename: Naoya
authors.initials: N
authors.lastname: Yamashita
authors.forename: Bedrich
authors.initials: B
authors.lastname: Mosinger
authors.forename: Arpita
authors.initials: A
authors.lastname: Roy
authors.forename: Mari
authors.initials: M
authors.lastname: Miyazaki
authors.forename: Kozue
authors.initials: K
authors.lastname: Ugajin
authors.forename: Fumio
authors.initials: F
authors.lastname: Nakamura
authors.forename: Yukio
authors.initials: Y
authors.lastname: Sasaki
authors.forename: Kazuhiko
authors.initials: K
authors.lastname: Yamaguchi
authors.forename: Pappachan
authors.initials: P
authors.lastname: Kolattukudy
authors.forename: Yoshio
authors.initials: Y
authors.lastname: Goshima
mesh_terms: D000581:Amidohydrolases / Q000172:deficiency / Q000235:genetics / Q000378:metabolism*; D000818:Animals; D000831:Animals, Newborn; D019208:Brain-Derived Neurotrophic Factor / Q000494:pharmacology; D002478:Cells, Cultured; D002531:Cerebellum / Q000378:metabolism; D003712:Dendrites / Q000187:drug effects / Q000378:metabolism*; D057809:HEK293 Cells; D006801:Humans; D006867:Hydrolases; D007150:Immunohistochemistry; D036881:Long-Term Synaptic Depression / Q000187:drug effects / Q000502:physiology*; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D008869:Microtubule-Associated Proteins; D009473:Neuronal Plasticity / Q000187:drug effects / Q000502:physiology*; D016133:Polymerase Chain Reaction; D011689:Purkinje Cells / Q000187:drug effects / Q000378:metabolism*; D020813:Receptor, trkB / Q000378:metabolism*; D009435:Synaptic Transmission / Q000187:drug effects / Q000502:physiology*
chemical_list: D019208:Brain-Derived Neurotrophic Factor; D008869:Microtubule-Associated Proteins; D020813:Receptor, trkB; C501733:Dpysl5 protein, mouse; D006867:Hydrolases; D000581:Amidohydrolases