Mice Lacking Brain-Derived Serotonin Have Altered Swallowing Function

The intricate sensorimotor neural circuits that control swallowing are heavily reliant on serotonin (5-hydroxytryptamine [5-HT]); however, the impact of 5-HT deficiency on swallow function remains largely unexplored. We investigated this using mice deficient in tryptophan-hydroxylase-2 (TPH2), the e...

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Bibliographic Details
Published in:Otolaryngology-head and neck surgery 2019-09, Vol.161 (3), p.468-471
Main Authors: Haney, Megan M., Sinnott, Joseph, Osman, Kate L., Deninger, Ian, Andel, Ellyn, Caywood, Victoria, Mok, Alexis, Ballenger, Brayton, Cummings, Kevin, Thombs, Lori, Lever, Teresa E.
Format: Article
Language:English
Subjects:
5‐hydroxytryptamine (5‐HT)
amyotrophic lateral sclerosis (ALS)
Animals
Brain Chemistry
Deglutition Disorders - etiology
Female
Male
Mice
mouse model
Serotonin - deficiency
Serotonin - isolation & purification
tryptophan hydroxylase (TPH)
videofluoroscopy
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Summary:The intricate sensorimotor neural circuits that control swallowing are heavily reliant on serotonin (5-hydroxytryptamine [5-HT]); however, the impact of 5-HT deficiency on swallow function remains largely unexplored. We investigated this using mice deficient in tryptophan-hydroxylase-2 (TPH2), the enzyme catalyzing the rate-limiting step in 5-HT synthesis. Videofluoroscopy was utilized to characterize the swallowing function of TPH2 knockout (TPH2-/-) mice as compared with littermate controls (TPH2+/+). Results showed that 5-HT deficiency altered all 3 stages of swallowing. As compared with controls, TPH2-/- mice had significantly slower lick and swallow rates and faster esophageal transit times. Future studies with this model are necessary to determine if 5-HT replacement may rescue abnormal swallowing function. If so, supplemental 5-HT therapy may have vast applications for a large population of patients with a variety of neurologic disorders resulting in life-diminishing dysphagia, particularly amyotrophic lateral sclerosis and Parkinson’s disease, for which 5-HT deficiency is implicated in the disease pathogenesis.
ISSN:0194-5998
1097-6817
DOI:10.1177/0194599819846109