title: Glia induce dendritic growth in cultured sympathetic neurons by modulating the balance between bone morphogenetic proteins (BMPs) and BMP antagonists.
abstract: Dendritic growth in cultured sympathetic neurons requires specific trophic interactions. Previous studies have demonstrated that either coculture with glia or exposure to recombinant bone morphogenetic proteins (BMPs) is both necessary and sufficient to induce dendrite formation. These observations led us to test the hypothesis that BMPs mediate glial-induced dendritic growth. In situ hybridization and immunocytochemical studies indicate that the spatiotemporal expression of BMP5, -6, and -7 in rat superior cervical ganglia (SCG) is consistent with their proposed role in dendritogenesis. In vitro, both SCG glia and neurons were found to express BMP mRNA and protein when grown in the presence or absence of the other cell type. However, addition of ganglionic glia to cultured sympathetic neurons causes a marked increase in BMP proteins coincident with a significant decrease in follistatin and noggin. Functional assays indicate that glial-induced dendritic growth is significantly reduced by BMP7 antibodies and completely inhibited by exogenous noggin and follistatin. These data suggest that glia influence the rapid perinatal expansion of the dendritic arbor in sympathetic neurons by increasing BMP activity via modulation of the balance between BMPs and their antagonists.
authors.affiliation: Department of Environmental Health Sciences, Johns Hopkins University Bloomberg School of Public Health, Baltimore, Maryland 21205-2179, USA. plein@jhsph.edu
authors.forename: Pamela J
authors.initials: PJ
authors.lastname: Lein
authors.forename: Hiroko Nagasawa
authors.initials: HN
authors.lastname: Beck
authors.forename: Vidya
authors.initials: V
authors.lastname: Chandrasekaran
authors.forename: Patrick J
authors.initials: PJ
authors.lastname: Gallagher
authors.forename: Hui-Ling
authors.initials: HL
authors.lastname: Chen
authors.forename: Yuan
authors.initials: Y
authors.lastname: Lin
authors.forename: Xin
authors.initials: X
authors.lastname: Guo
authors.forename: Paul L
authors.initials: PL
authors.lastname: Kaplan
authors.forename: Henri
authors.initials: H
authors.lastname: Tiedge
authors.forename: Dennis
authors.initials: D
authors.lastname: Higgins
mesh_terms: D021581:Active Transport, Cell Nucleus / Q000502:physiology; D000818:Animals; D000906:Antibodies / Q000494:pharmacology; D019485:Bone Morphogenetic Proteins / Q000037:antagonists & inhibitors / Q000235:genetics / Q000378:metabolism*; D002352:Carrier Proteins; D002455:Cell Division / Q000502:physiology; D002478:Cells, Cultured; D018920:Coculture Techniques; D004268:DNA-Binding Proteins / Q000378:metabolism; D003712:Dendrites / Q000187:drug effects / Q000502:physiology*; D015536:Down-Regulation / Q000502:physiology; D038681:Follistatin / Q000235:genetics / Q000378:metabolism; D006801:Humans; D017403:In Situ Hybridization; D009457:Neuroglia / Q000166:cytology / Q000187:drug effects / Q000502:physiology*; D009474:Neurons / Q000166:cytology / Q000187:drug effects / Q000378:metabolism*; D011506:Proteins / Q000235:genetics / Q000378:metabolism*; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D015398:Signal Transduction / Q000187:drug effects / Q000502:physiology; D051785:Smad Proteins; D013564:Sympathetic Nervous System / Q000166:cytology / Q000187:drug effects / Q000378:metabolism*; D015534:Trans-Activators / Q000378:metabolism; D015854:Up-Regulation / Q000502:physiology; D000099176:Noggin Protein
chemical_list: D000906:Antibodies; D019485:Bone Morphogenetic Proteins; D002352:Carrier Proteins; D004268:DNA-Binding Proteins; D038681:Follistatin; D011506:Proteins; D012333:RNA, Messenger; D051785:Smad Proteins; D015534:Trans-Activators; D000099176:Noggin Protein