title: Hilar mossy cells share developmental influences with dentate granule neurons.
abstract: Mossy cells are the major class of excitatory neurons in the dentate hilus. Although mossy cells are involved in a range of physiological and pathological conditions, very little is known about their ontogeny. To gain insight into this issue, we first determined the developmental stage at which mossy cells can be reliably identified with the molecular markers calretinin and GluR2/3 and found that hilar mossy cells were first identifiable around the end of the 1st postnatal week. Birthdating studies combined with staining for these markers revealed that the appearance of mossy cells coincided with the first wave of dentate granule cell production during mid-gestation. Since mossy cells are born as the first granule cells are produced and it is believed that mossy cells originate from the neuroepithelium adjacent to the dentate progenitor zone, we examined to what extent the development of mossy cells is controlled by the same molecular pathways as that of granule cells. To do this, we analyzed the production of mossy cells in Lef1 and NeuroD mutant animals, in which granule cell production is disrupted during precursor proliferation or neuronal differentiation, respectively. The production of mossy cells was almost entirely lost in both mutants. Collectively, these data suggests that hilar mossy cells, unlike CA subfield pyramidal cells, are influenced by many of the same developmental cues as dentate granule cells.
authors.affiliation: Department of Neurology and Programs in Neuroscience and Developmental Biology, University of California, San Francisco, CA 94143-2722, USA.
authors.forename: Guangnan
authors.initials: G
authors.lastname: Li
authors.forename: Omri
authors.initials: O
authors.lastname: Berger
authors.forename: Szu-Min
authors.initials: SM
authors.lastname: Han
authors.forename: Mercedes
authors.initials: M
authors.lastname: Paredes
authors.forename: Ni-Chi
authors.initials: NC
authors.lastname: Wu
authors.forename: Samuel J
authors.initials: SJ
authors.lastname: Pleasure
mesh_terms: D000818:Animals; D051792:Basic Helix-Loop-Helix Proteins / Q000235:genetics; D015415:Biomarkers / Q000378:metabolism*; D064032:Calbindin 2; D002455:Cell Division / Q000502:physiology; D018891:Dentate Gyrus / Q000166:cytology / Q000196:embryology / Q000254:growth & development; D051821:Lymphoid Enhancer-Binding Factor 1 / Q000235:genetics; D051379:Mice; D008810:Mice, Inbred C57BL; D008817:Mice, Mutant Strains; D019599:Mossy Fibers, Hippocampal / Q000378:metabolism*; D009419:Nerve Tissue Proteins / Q000235:genetics; D009474:Neurons / Q000166:cytology* / Q000378:metabolism; D017966:Pyramidal Cells / Q000166:cytology / Q000378:metabolism; D018091:Receptors, AMPA / Q000378:metabolism; D064030:S100 Calcium Binding Protein G / Q000378:metabolism
chemical_list: D051792:Basic Helix-Loop-Helix Proteins; D015415:Biomarkers; D064032:Calbindin 2; D051821:Lymphoid Enhancer-Binding Factor 1; D009419:Nerve Tissue Proteins; D018091:Receptors, AMPA; D064030:S100 Calcium Binding Protein G; C576511:Calb2 protein, mouse; C497574:Lef1 protein, mouse; C104723:glutamate receptor ionotropic, AMPA 3; C093564:Neurogenic differentiation factor 1; C104722:glutamate receptor ionotropic, AMPA 2