Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
2009-8-13
pubmed:abstractText
Semaphorin-3A (Sema3A) is an attractive guidance molecule for cortical apical dendrites. To elucidate the role of Sema3A in hippocampal dendritic formation, we examined the Sema3A expression pattern in the perinatal hippocampal formation and analyzed hippocampal dendrites of the brains from young adult sema3A mutant mice. Sema3A protein was predominantly expressed in the hippocampal plate and the inner marginal zone at the initial period of apical dendritic growth. Neuropilin-1 and plexin-A, the receptor components for Sema3A, were also localized in the same regions. The Golgi impregnation method revealed that in wildtype mice more than 90% of hippocampal CA1 pyramidal neurons extended a single trunk or apical trunks bifurcated in stratum radiatum. Seven percent of the pyramidal neurons showed proximal bifurcation of apical trunks in stratum pyramidale or at the border of the stratum pyramidale and stratum radiatum. In sema3A mutant mice, proximally bifurcated apical dendrites were increased to 32%, while the single apical dendritic pyramidal neurons were decreased. We designate this phenotype in sema3A mutant mice as "proximal bifurcation." In the dissociated culture system, approximately half of the hippocampal neurons from wildtype mice resembled pyramidal neurons, which possess a long, thick, and tapered dendrite. In contrast, only 30% of the neurons from sema3A mutants exhibited pyramidal-like morphology. Proximal bifurcation of CA1 pyramidal neurons was also increased in the mutant mice of p35, an activator of cyclin-dependent kinase 5 (Cdk5). Thus, Sema3A may facilitate the initial growth of CA1 apical dendrites via the activation of p35/Cdk5, which may in turn signal hippocampal development.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
1096-9861
pubmed:author
pubmed:issnType
Electronic
pubmed:day
10
pubmed:volume
516
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
360-75
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed-meshheading:19655386-Animals, pubmed-meshheading:19655386-Antisense Elements (Genetics), pubmed-meshheading:19655386-Cells, Cultured, pubmed-meshheading:19655386-Cyclin-Dependent Kinase 5, pubmed-meshheading:19655386-Dendrites, pubmed-meshheading:19655386-Golgi Apparatus, pubmed-meshheading:19655386-Hippocampus, pubmed-meshheading:19655386-Humans, pubmed-meshheading:19655386-Image Processing, Computer-Assisted, pubmed-meshheading:19655386-Immunohistochemistry, pubmed-meshheading:19655386-In Situ Hybridization, pubmed-meshheading:19655386-Mice, pubmed-meshheading:19655386-Mice, Inbred C57BL, pubmed-meshheading:19655386-Microtubule-Associated Proteins, pubmed-meshheading:19655386-Mutation, pubmed-meshheading:19655386-Phenotype, pubmed-meshheading:19655386-Pyramidal Cells, pubmed-meshheading:19655386-Semaphorin-3A, pubmed-meshheading:19655386-Signal Transduction, pubmed-meshheading:19655386-Tumor Suppressor Protein p53
pubmed:year
2009
pubmed:articleTitle
Increased proximal bifurcation of CA1 pyramidal apical dendrites in sema3A mutant mice.
pubmed:affiliation
Yokohama City University Graduate School of Medicine, Department of Molecular Pharmacology and Neurobiology, 3-9, Fukuura, Kanazawa-ku, Yokohama, Kanagawa 236-0004, Japan. f-nakamura@umin.ac.jp
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't