Presentation Details
| Neurogenesis in the olfactory epithelium of adult zebrafish following olfactory bulb lesions Rebecca Post, Nereyda Sanchez-Gama, Lexus Putt, Erika Calvo-Ochoa. Hope College, Holland, MI, USA |
Abstract
Zebrafish (Danio rerio) are one of the few vertebrates that can repair brain lesions and generate new neurons (i.e., neurogenesis) throughout their lifespan. In particular, the olfactory system, consisting of the olfactory bulb (OB) and the olfactory epithelium (OE), exhibits extensive neuroplasticity, and repair mechanisms – including neurogenesis – in response to damage. The OE has two stem cell populations that are responsible for constitutive turnover and post-damage regeneration of olfactory sensory neurons (OSNs): and globose basal cells (GBCs) and horizontal basal cells (HBCs),), respectively. While it is known that HBCs are dormant and that direct injury to the OE activates their proliferation, less is known about their role in regenerating the OE after damage of the OB. To study this, in this work we use a model of retrograde degeneration of the OE by excitotoxic lesions in the OB using quinolinic acid (QA) in adult zebrafish. We have established that these lesions cause neurodegeneration in the OE and olfactory functional deficits. Neurogenesis supports recovery by 21 days post-lesion (dpl). In this work, we study recovery and regeneration processes taking place during early post-lesion recovery at 1-, 6-, 24-, and 72- hr post lesion (hpl). We performed immunohistochemical examinations of the olfactory epithelium and assessed markers of cell proliferation, stem cell activation, and neurogenesis. Our results provide a comprehensive time-course characterization of post-damage cell proliferation and neurogenesis in the olfactory epithelium of adult zebrafish. This work contributes to the understanding of basic biological mechanisms underlying neurogenesis in adult vertebrates, with the potential to inform therapeutic strategies to alleviate olfactory dysfunction in human patients.
No part of this publication may be reproduced, distributed, or transmitted in any form or by any means, including photocopying, recording, or other electronic or mechanical methods, without the prior written permission of the author.
No part of this publication may be reproduced, distributed, or transmitted in any form or by any means, including photocopying, recording, or other electronic or mechanical methods, without the prior written permission of the author.