ArticleNeural development2012
Olfactory discrimination largely persists in mice with defects in odorant receptor expression and axon guidance.
Article in Neural development, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 16 citations in OpenAlex.
- CXCR4 Coordinates Long-Term Olfactory Epithelial Regeneration and Cellular Stress Response After Injury.Molecular neurobiology · 2026Article
- Insights into Convergent Evolution From Studying Amino Acid Patterns in Independent Lineages of Birds.Genome biology and evolution · 2025Article
- Dense and Persistent Odor Representations in the Olfactory Bulb of Awake Mice.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- Adaptive olfactory circuitry restores function despite severe olfactory bulb degeneration.Current biology : CB · 2023Article
- Learning peptide recognition rules for a low-specificity protein.Protein science : a publication of the Protein Society · 2020Article
- AutonoMouse: High throughput operant conditioning reveals progressive impairment with graded olfactory bulb lesions.PloS one · 2019Article
- Conservation of Specificity in Two Low-Specificity Proteins.Biochemistry · 2018Article
- Deletion of Type 3 Adenylyl Cyclase Perturbs the Postnatal Maturation of Olfactory Sensory Neurons and Olfactory Cilium Ultrastructure in Mice.Frontiers in cellular neuroscience · 2017Article
- Transcriptome study of differential expression in schizophrenia.Human molecular genetics · 2013Article
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Authors and funding
7 authors at 2 institutions in 2 countries.
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Abstract
backgroundThe defining feature of the main olfactory system in mice is that each olfactory sensory neuron expresses only one of more than a thousand different odorant receptor genes. Axons expressing the same odorant receptor converge onto a small number of targets in the olfactory bulb such that each glomerulus is made up of axon terminals expressing just one odorant receptor. It is thought that this precision in axon targeting is required to maintain highly refined odor discrimination. We previously showed that β3GnT2(-/-) mice have severe developmental and axon guidance defects. The phenotype of these mice is similar to adenylyl cyclase 3 (AC3) knockout mice largely due to the significant down-regulation of AC3 activity in β3GnT2(-/-) neurons.
resultsMicroarray analysis reveals that nearly one quarter of all odorant receptor genes are down regulated in β3GnT2(-/-) mice compared to controls. Analysis of OR expression by quantitative PCR and in situ hybridization demonstrates that the number of neurons expressing some odorant receptors, such as mOR256-17, is increased by nearly 60% whereas for others such as mOR28 the number of neurons is decreased by more than 75% in β3GnT2(-/-) olfactory epithelia. Analysis of axon trajectories confirms that many axons track to inappropriate targets in β3GnT2(-/-) mice, and some glomeruli are populated by axons expressing more than one odorant receptor. Results show that mutant mice perform nearly as well as control mice in an odor discrimination task. In addition, in situ hybridization studies indicate that the expression of several activity dependent genes is unaffected in β3GnT2(-/-) olfactory neurons.
conclusionsResults presented here show that many odorant receptors are under-expressed in β3GnT2(-/-) mice and further demonstrate that additional axon subsets grow into inappropriate targets or minimally innervate glomeruli in the olfactory bulb. Odor evoked gene expression is unchanged and β3GnT2(-/-) mice exhibit a relatively small deficit in their ability to discriminate divergent odors. Results suggest that despite the fact that β3GnT2(-/-) mice have decreased AC3 activity, decreased expression of many ORs, and display many axon growth and guidance errors, odor-evoked activity in cilia of mutant olfactory neurons remains largely intact.
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