Presentation Details
| Inflammation is necessary for regeneration and repair of the damaged olfactory system of adult zebrafish Lexus Putt, Olivia Wiley, Erika Calvo-Ochoa. Hope College, Holland, MI, USA |
Abstract
Zebrafish are an ideal model for studying injury-induced neural repair because they robustly regenerate neurons in both the central and peripheral nervous systems. Their olfactory system, composed of the olfactory bulb (OB) and olfactory epithelium (OE), is highly neurogenic and analogous to that of humans. In zebrafish, neuroinflammation supports regeneration after injury, in contrast to mammals. Rather than classic stellate astrocytes, the zebrafish brain contains radial glial–like astroglia and olfactory ensheathing cells that promote repair. Although inflammation is essential for brain regeneration, its role in OE repair remains poorly understood. We used a model of retrograde degeneration induced by excitotoxic OB lesions with quinolinic acid (QA) in adult zebrafish. Previous work showed that QA lesions cause OE neurodegeneration and olfactory deficits, followed by neurogenesis and functional recovery. Here, we examined inflammatory responses during early recovery at 1, 6, 24, and 72 hours post-lesion (hpl). Immunohistochemistry was used to assess inflammatory markers, including GFAP (glial fibrillary acidic protein; astroglial cells) and Lcp1 (lymphocyte cytosolic protein 1; leukocytes). To test the functional role of inflammation, we treated animals with the anti-inflammatory drug pranlukast, a cysteinyl leukotriene receptor antagonist.QA lesions increased leukocyte density in both the OB and OE; this response was reduced by pranlukast in the OB but not in the OE. Astroglial activity exhibited a bimodal pattern during acute recovery. Notably, anti-inflammatory treatment reduced cell proliferation in the OE. Together, these findings shed light on inflammatory processes following olfactory system injury and highlight their contribution to neural repair in adult vertebrates.
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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.
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