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Taste Bud-Derived BDNF Is Required to Maintain Normal Amounts of Innervation to Adult Taste Buds.

Meng L, Ohman-Gault L, Ma L, Krimm RF - eNeuro (2015)

Bottom Line: We then tested the idea that that the taste bud was the source of this BDNF by reducing Bdnf levels specifically in the lingual epithelium and taste buds.Taste buds were confirmed as the source of BDNF regulating innervation.We conclude that BDNF expressed in taste receptor cells is required to maintain normal levels of innervation in adulthood.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Anatomical Sciences and Neurobiology, University of Louisville School of Medicine , Louisville, Kentucky 40292.

ABSTRACT
Gustatory neurons transmit chemical information from taste receptor cells, which reside in taste buds in the oral cavity, to the brain. As adult taste receptor cells are renewed at a constant rate, nerve fibers must reconnect with new taste receptor cells as they arise. Therefore, the maintenance of gustatory innervation to the taste bud is an active process. Understanding how this process is regulated is a fundamental concern of gustatory system biology. We speculated that because brain-derived neurotrophic factor (BDNF) is required for taste bud innervation during development, it might function to maintain innervation during adulthood. If so, taste buds should lose innervation when Bdnf is deleted in adult mice. To test this idea, we first removed Bdnf from all cells in adulthood using transgenic mice with inducible CreERT2 under the control of the Ubiquitin promoter. When Bdnf was removed, approximately one-half of the innervation to taste buds was lost, and taste buds became smaller because of the loss of taste bud cells. Individual taste buds varied in the amount of innervation each lost, and those that lost the most innervation also lost the most taste bud cells. We then tested the idea that that the taste bud was the source of this BDNF by reducing Bdnf levels specifically in the lingual epithelium and taste buds. Taste buds were confirmed as the source of BDNF regulating innervation. We conclude that BDNF expressed in taste receptor cells is required to maintain normal levels of innervation in adulthood.

No MeSH data available.


Related in: MedlinePlus

Taste receptor cells were quantified in whole taste buds from Bdnflox/- (A) and CreER Bdnflox/-(D) mice, ten weeks after tamoxifen administration. Taste buds were imaged with the high-resolution X–Y plane in cross-section (B, E), such that individual PLCβ2-positive (red, arrow) and Car4-positive (white, arrowheads) could be quantified by following each cell from the taste pore to the basal region of the bud (C, F). Cytokeratin-8-positive cells (green) could also be quantified (B, E). Scale bar, 10µm.
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Figure 5: Taste receptor cells were quantified in whole taste buds from Bdnflox/- (A) and CreER Bdnflox/-(D) mice, ten weeks after tamoxifen administration. Taste buds were imaged with the high-resolution X–Y plane in cross-section (B, E), such that individual PLCβ2-positive (red, arrow) and Car4-positive (white, arrowheads) could be quantified by following each cell from the taste pore to the basal region of the bud (C, F). Cytokeratin-8-positive cells (green) could also be quantified (B, E). Scale bar, 10µm.

Mentions: Because taste bud size was reduced, we wished to determine if one particular taste receptor cell type was influenced more than others were. Taste receptor cells with the G-protein-coupled receptors for sweet, bitter, and umami were labeled with anti-PLCβ2, whereas another type that responds to acid labels with anti-Car4. Taste buds were imaged in whole mounts, so that all taste cells of a given type could be reported in whole numbers rather than percentages (Fig. 5). Because there were no differences in taste bud size in the control groups we compared one control group (Bdnflox/-) with the experimental group (CreERT2 Bdnflox/-), both of which received tamoxifen. There was no difference between genotypes in the number of PLCβ2-positive (Bdnflox/- mice = 11.8 ± 0.56 vs CreERT2 Bdnflox/- = 11.3 ± 1.2) or Car4-positive (Bdnflox/- mice = 2.78 ± 0.55 vs CreERT2 Bdnflox/- = 2.0 ± 0.38) taste receptor cells. We also labeled and quantified the cytokeratin 8 positive cells; there was a slight decrease in CreERT2 Bdnflox/- (30 ± 1.03) compared with Bdnflox/- (34.4 ± 1.52; p < 0.03). We conclude that the loss of taste cells is not due to loss of a specific taste bud cell type.


Taste Bud-Derived BDNF Is Required to Maintain Normal Amounts of Innervation to Adult Taste Buds.

Meng L, Ohman-Gault L, Ma L, Krimm RF - eNeuro (2015)

Taste receptor cells were quantified in whole taste buds from Bdnflox/- (A) and CreER Bdnflox/-(D) mice, ten weeks after tamoxifen administration. Taste buds were imaged with the high-resolution X–Y plane in cross-section (B, E), such that individual PLCβ2-positive (red, arrow) and Car4-positive (white, arrowheads) could be quantified by following each cell from the taste pore to the basal region of the bud (C, F). Cytokeratin-8-positive cells (green) could also be quantified (B, E). Scale bar, 10µm.
© Copyright Policy - open-access
Related In: Results  -  Collection

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Show All Figures
getmorefigures.php?uid=PMC4697083&req=5

Figure 5: Taste receptor cells were quantified in whole taste buds from Bdnflox/- (A) and CreER Bdnflox/-(D) mice, ten weeks after tamoxifen administration. Taste buds were imaged with the high-resolution X–Y plane in cross-section (B, E), such that individual PLCβ2-positive (red, arrow) and Car4-positive (white, arrowheads) could be quantified by following each cell from the taste pore to the basal region of the bud (C, F). Cytokeratin-8-positive cells (green) could also be quantified (B, E). Scale bar, 10µm.
Mentions: Because taste bud size was reduced, we wished to determine if one particular taste receptor cell type was influenced more than others were. Taste receptor cells with the G-protein-coupled receptors for sweet, bitter, and umami were labeled with anti-PLCβ2, whereas another type that responds to acid labels with anti-Car4. Taste buds were imaged in whole mounts, so that all taste cells of a given type could be reported in whole numbers rather than percentages (Fig. 5). Because there were no differences in taste bud size in the control groups we compared one control group (Bdnflox/-) with the experimental group (CreERT2 Bdnflox/-), both of which received tamoxifen. There was no difference between genotypes in the number of PLCβ2-positive (Bdnflox/- mice = 11.8 ± 0.56 vs CreERT2 Bdnflox/- = 11.3 ± 1.2) or Car4-positive (Bdnflox/- mice = 2.78 ± 0.55 vs CreERT2 Bdnflox/- = 2.0 ± 0.38) taste receptor cells. We also labeled and quantified the cytokeratin 8 positive cells; there was a slight decrease in CreERT2 Bdnflox/- (30 ± 1.03) compared with Bdnflox/- (34.4 ± 1.52; p < 0.03). We conclude that the loss of taste cells is not due to loss of a specific taste bud cell type.

Bottom Line: We then tested the idea that that the taste bud was the source of this BDNF by reducing Bdnf levels specifically in the lingual epithelium and taste buds.Taste buds were confirmed as the source of BDNF regulating innervation.We conclude that BDNF expressed in taste receptor cells is required to maintain normal levels of innervation in adulthood.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Anatomical Sciences and Neurobiology, University of Louisville School of Medicine , Louisville, Kentucky 40292.

ABSTRACT
Gustatory neurons transmit chemical information from taste receptor cells, which reside in taste buds in the oral cavity, to the brain. As adult taste receptor cells are renewed at a constant rate, nerve fibers must reconnect with new taste receptor cells as they arise. Therefore, the maintenance of gustatory innervation to the taste bud is an active process. Understanding how this process is regulated is a fundamental concern of gustatory system biology. We speculated that because brain-derived neurotrophic factor (BDNF) is required for taste bud innervation during development, it might function to maintain innervation during adulthood. If so, taste buds should lose innervation when Bdnf is deleted in adult mice. To test this idea, we first removed Bdnf from all cells in adulthood using transgenic mice with inducible CreERT2 under the control of the Ubiquitin promoter. When Bdnf was removed, approximately one-half of the innervation to taste buds was lost, and taste buds became smaller because of the loss of taste bud cells. Individual taste buds varied in the amount of innervation each lost, and those that lost the most innervation also lost the most taste bud cells. We then tested the idea that that the taste bud was the source of this BDNF by reducing Bdnf levels specifically in the lingual epithelium and taste buds. Taste buds were confirmed as the source of BDNF regulating innervation. We conclude that BDNF expressed in taste receptor cells is required to maintain normal levels of innervation in adulthood.

No MeSH data available.


Related in: MedlinePlus