Presentation Details
| Subpopulations of gustatory neurons differ in their sensitivity to BDNF Mara J.Stout, Alvine J.Smith, Robin F.Krimm. University of Louisville, Louisville, KY, USA |
Abstract
Peripheral taste neuron survival and targeting is dependent on expression of neurotrophic factors such as brain-derived neurotrophic factor (BDNF). When BDNF is overexpressed (OE) in basal epithelium of tongue and skin, the number of neurons increases in the geniculate ganglion, but in the tongue these neurons fail to innervate the correct location. Taste neurons are genetically and functionally diverse, and genetic subpopulations could vary in the responsiveness to BDNF. To determine if genetic populations are impacted differently by BDNF overexpression, we investigated the defined proenkephalin (Penk+) expressing population and compared results to the full population defined by expression of the transcription factor paired like homeobox 2B (Phox2b+) in wildtype and OE mice. We found that the number of Penk+ neurons decreased in OE mice (p<0.05) whereas the Phox2b+ neurons remained unchanged. We then hypothesized that another genetic subpopulation increases in OE mice, but so far, have found no such population. The decrease in Penk+ geniculate neurons could be due to disrupted target innervation. Consistent with this possibility, by P60, innervation of fungiform taste buds by Penk+ neurons is disrupted when compared to Phox2b+ neurons. Specifically, the percentage of taste buds innervated by Penk+ fibers decreases in OE mice (p<0.05) whereas Phox2b+ innervation remains unchanged. In addition, the volume occupied by Penk+ fibers in the taste bud decreased significantly (p<0.05) in OE mice compared to controls. Whereas the Phox2b+ nerve fiber volume did not decrease. Our data suggests that subpopulations of taste neurons are impacted differently by BDNF overexpression. Thus, different gustatory neuron types are regulated differentially by developmental factors.
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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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