4.0 Article

Single or Repeated Ablation of Mouse Olfactory Epithelium by Methimazole

Journal

BIO-PROTOCOL
Volume 11, Issue 8, Pages -

Publisher

BIO-PROTOCOL
DOI: 10.21769/BioProtoc.3983

Keywords

Olfactory epithelium; Methimazole; Lesion; Regeneration; Tissue stem cell; Metaplasia

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Funding

  1. Swedish Brain Foundation [FO20180195]
  2. Technical-natural science faculty at Umea University

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Olfactory sensory neurons in the nasal olfactory epithelium are directly exposed to environmental insults, making them a useful model for studying neurogenesis and differentiation. Compounds like methimazole can cause olfactotoxicity as a side effect, offering a method for OE ablation and regeneration studies. Single or repeated methimazole administration can be used to investigate neuroepithelial regeneration, stem cell activation, tissue stem cell exhaustion, and tissue metaplasia in the OE.
Odor-detecting olfactory sensory neurons residing in the nasal olfactory epithelium (OE) are the only neurons in direct contact with the external environment. As a result, these neurons are subjected to chemical, physical, and infectious insults, which may be the underlying reason why neurogenesis occurs in the OE of adult mammals. This feature makes the OE a useful model for studying neurogenesis and neuronal differentiation, with the possibility for systemic as well as local administration of various compounds and infectious agents that may interfere with these cellular processes. Several different chemical compounds have been shown to cause toxic injury to the OE, which can be used for OE ablation. We, and others, have found that the systemic administration of the hyperthyroid drug, methimazole, reliably causes olfactotoxicity as a side effect. Here, we outline an OE lesioning protocol for single or repeated ablation by methimazole. A single methimazole administration can be used to study neuroepithelial regeneration and stem cell activation, while repeated ablation and regeneration of OE enable the study of tissue stem cell exhaustion and generation of tissue metaplasia.

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