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1.
Mol Cell Neurosci ; 32(1-2): 1-14, 2006.
Article in English | MEDLINE | ID: mdl-16531066

ABSTRACT

There is an overall topographic connectivity in the axonal projections of olfactory sensory neurons from the olfactory epithelium (OE) to the olfactory bulb (OB). The molecular determinants of this overall topographic OE-OB connectivity are not known. For 20 years, the intriguing expression pattern of the olfactory cell adhesion molecule (OCAM) has made it the leading candidate as determinant of overall topographic OE-OB connectivity. Here, we have generated a strain of OCAM knockout mice by gene targeting. There were no obvious alterations in the distribution of olfactory sensory neurons within the OE or in the coalescence of axons into specific glomeruli. However, the compartmental organization of dendrites and axons within the glomeruli was disrupted. Surprisingly, the mutant mice exhibited an increase in olfactory acuity; they appeared to have a better sense of smell. Thus, despite its striking expression pattern, OCAM is not essential for overall topographic OE-OB connectivity. Instead, OCAM is required for establishing or maintaining the compartmental organization and the segregation of axodendritic and dendrodendritic synapses within glomeruli.


Subject(s)
Axons/metabolism , Cell Differentiation/genetics , Dendrites/metabolism , Neural Cell Adhesion Molecules/genetics , Olfactory Bulb/abnormalities , Olfactory Receptor Neurons/abnormalities , Animals , Axons/ultrastructure , Cell Communication/genetics , Dendrites/ultrastructure , Female , Gene Expression Regulation, Developmental/genetics , Male , Mice , Mice, Inbred C57BL , Mice, Knockout , Mice, Transgenic , Neural Cell Adhesion Molecules/deficiency , Neuronal Plasticity/genetics , Neuropil/metabolism , Neuropil/ultrastructure , Olfactory Bulb/cytology , Olfactory Bulb/metabolism , Olfactory Nerve/abnormalities , Olfactory Nerve/cytology , Olfactory Nerve/metabolism , Olfactory Receptor Neurons/cytology , Olfactory Receptor Neurons/metabolism , Presynaptic Terminals/metabolism , Presynaptic Terminals/ultrastructure , Smell/genetics
2.
Mol Cell Neurosci ; 27(1): 44-58, 2004 Sep.
Article in English | MEDLINE | ID: mdl-15345242

ABSTRACT

Rett syndrome (RTT) is a severe neurodevelopmental disorder with features of autism that results from mutation of the gene encoding the transcriptional repressor methyl-CpG binding protein (MECP2). The consequences of loss of a transcription factor may be complex, affecting the expression of many proteins, thus limiting understanding of this class of diseases and impeding therapeutic strategies. This is true for RTT. Neither the cell biological mechanism(s) nor the developmental stage affected by MECP2 deficiency is known. In vivo analysis of the olfactory system demonstrates that Mecp2 deficiency leads to a transient delay in the terminal differentiation of olfactory neurons. This delay in maturation disrupts axonal targeting in the olfactory bulb, resulting in abnormal axonal projections, subglomerular disorganization, and a persistent reduction in glomerular size. These results indicate a critical cell biological function for Mecp2 in mediating the final stages of neuronal development.


Subject(s)
Chromosomal Proteins, Non-Histone/genetics , DNA-Binding Proteins/genetics , Neurons/metabolism , Olfactory Bulb/abnormalities , Olfactory Pathways/abnormalities , Olfactory Receptor Neurons/abnormalities , Repressor Proteins/genetics , Animals , Biomarkers , Cell Differentiation/genetics , Disease Models, Animal , GAP-43 Protein/metabolism , Gene Expression Regulation, Developmental/genetics , Growth Cones/metabolism , Growth Cones/ultrastructure , Methyl-CpG-Binding Protein 2 , Mice , Mice, Knockout , Nerve Tissue Proteins/metabolism , Neurons/ultrastructure , Neuropil/cytology , Neuropil/metabolism , Olfactory Bulb/cytology , Olfactory Bulb/metabolism , Olfactory Marker Protein , Olfactory Pathways/cytology , Olfactory Pathways/metabolism , Olfactory Receptor Neurons/cytology , Olfactory Receptor Neurons/metabolism , Rett Syndrome/genetics , Rett Syndrome/metabolism , Synapses/genetics , Synapses/metabolism
3.
Neuron ; 35(4): 681-96, 2002 Aug 15.
Article in English | MEDLINE | ID: mdl-12194868

ABSTRACT

An olfactory sensory neuron (OSN) expresses selectively one member from a repertoire of approximately 1000 odorant receptor (OR) genes and projects its axon to a specific glomerulus in the olfactory bulb. Both processes are here recapitulated by MOR23 and M71 OR minigenes, introduced into mice. Minigenes of 9 kb and as short as 2.2 kb are selectively expressed by neurons that do not coexpress the endogenous gene but coproject their axons to the same glomeruli. Deletion of a 395 bp upstream region in the MOR23 minigene abolishes expression. In this region we recognize sequence motifs conserved in many OR genes. Transgenic lines expressing the OR in ectopic epithelial zones form ectopic glomeruli, which also receive input from OSNs expressing the cognate endogenous receptor. This suggests a recruitment through homotypic interactions between OSNs expressing the same OR.


Subject(s)
Cell Differentiation/genetics , Gene Expression Regulation, Developmental/genetics , Growth Cones/metabolism , Olfactory Bulb/abnormalities , Olfactory Pathways/abnormalities , Olfactory Receptor Neurons/abnormalities , Receptors, Odorant/genetics , Animals , Base Sequence/genetics , Binding Sites/genetics , Gene Deletion , Genes, Reporter/genetics , Growth Cones/ultrastructure , Homeodomain Proteins/genetics , Introns/genetics , Mice , Mice, Inbred C57BL , Mice, Transgenic , Molecular Sequence Data , Olfactory Bulb/cytology , Olfactory Bulb/metabolism , Olfactory Pathways/cytology , Olfactory Pathways/metabolism , Olfactory Receptor Neurons/cytology , Olfactory Receptor Neurons/metabolism , Transgenes/genetics
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