Mice Lacking Brain‐Derived Serotonin Have Altered Swallowing Function

Haney, Megan M.; Sinnott, Joseph Dalby; Osman, Kate L; Deninger, Ian; Andel, Ellyn; Caywood, Victoria; Mok, Alexis; Ballenger, Brayton; Cummings, Kevin J.; Thombs, Lori A.; Lever, Teresa E.

doi:10.1177/0194599819846109

Cited by 19 publications

(12 citation statements)

References 23 publications

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“…Contrary to glutamate effects, QPZ injection in vivo produced single or “isolated” swallows and increased the swallow rate over a long period [ 5 , 19 ], which represents an optimal condition to study swallow-breathing interaction, and a good alternative method to evoke swallowing [ 8 ]. In agreement with the role of bulbar serotonergic control of swallowing [ 5 ], mice with central 5-HT deficiency had lower swallow rates than control animals [ 20 ]. However, inhibitory effects of serotonergic agonists on swallowing, including QPZ, have also been reported [ 21 , 22 ].…”

Section: Introductionsupporting

confidence: 57%

Quipazine Elicits Swallowing in the Arterially Perfused Rat Preparation: A Role for Medullary Raphe Nuclei?

Bergé-Laval¹,

Gestreau²

2020

IJMS

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Pharmacological neuromodulation of swallowing may represent a promising therapeutic option to treat dysphagia. Previous studies suggested a serotonergic control of swallowing, but mechanisms remain poorly understood. Here, we investigated the effects of the serotonergic agonist quipazine on swallowing, using the arterially perfused working heart-brainstem (in situ) preparation in rats. Systemic injection of quipazine produced single swallows with motor patterns and swallow-breathing coordination similar to spontaneous swallows, and increased swallow rate with moderate changes in cardiorespiratory functions. Methysergide, a 5-HT2 receptor antagonist, blocked the excitatory effect of quipazine on swallowing, but had no effect on spontaneous swallow rate. Microinjections of quipazine in the nucleus of the solitary tract were without effect. In contrast, similar injections in caudal medullary raphe nuclei increased swallow rate without changes in cardiorespiratory parameters. Thus, quipazine may exert an excitatory effect on raphe neurons via stimulation of 5-HT2A receptors, leading to increased excitability of the swallowing network. In conclusion, we suggest that pharmacological stimulation of swallowing by quipazine in situ represents a valuable model for experimental studies. This work paves the way for future investigations on brainstem serotonergic modulation, and further identification of neural populations and mechanisms involved in swallowing and/or swallow-breathing interaction.

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Section: Introductionsupporting

confidence: 57%

Quipazine Elicits Swallowing in the Arterially Perfused Rat Preparation: A Role for Medullary Raphe Nuclei?

Bergé-Laval¹,

Gestreau²

2020

IJMS

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“…Moreover, polymorphisms in TPH2 are associated with addictive behaviors [73] and depression [74] in PD patients. Additionally, Tph2 KO mice, which have serotonin deficiency, present with systemic oxidative stress and lipidomic abnormalities [75], and swallowing dysfunction [76]. The alpha-D1 adrenergic receptor encoded by ADRA1D is also downregulated in the hippocampus of Alzheimer's disease and dementia with Lewy bodies patients [77], and noradrenergic impairment is present in PD patients as well [78].…”

Section: Discussionmentioning

confidence: 99%

Explorative Combined Lipid and Transcriptomic Profiling of Substantia Nigra and Putamen in Parkinson’s Disease

Brouwers

Wieringa

Martens³

2020

Cells

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Parkinson’s disease (PD) is characterized by the loss of dopaminergic neurons from the substantia nigra (SN) that project to the dorsal striatum (caudate-putamen). To better understand the molecular mechanisms underlying PD, we performed combined lipid profiling and RNA sequencing of SN and putamen samples from PD patients and age-matched controls. SN lipid analysis pointed to a neuroinflammatory component and included elevated levels of the endosomal lipid Bis (Monoacylglycero)Phosphate 42:8, while two of the three depleted putamen lipids were saturated sphingomyelin species. Remarkably, we observed gender-related differences in the SN and putamen lipid profiles. Transcriptome analysis revealed that the top-enriched pathways among the 354 differentially expressed genes (DEGs) in the SN were “protein folding” and “neurotransmitter transport”, and among the 261 DEGs from putamen “synapse organization”. Furthermore, we identified pathways, e.g., “glutamate signaling”, and genes, encoding, e.g., an angiotensin receptor subtype or a proprotein convertase, that have not been previously linked to PD. The identification of 33 genes that were common among the SN and putamen DEGs, which included the α-synuclein paralog β-synuclein, may contribute to the understanding of general PD mechanisms. Thus, our proof-of-concept data highlights new genes, pathways and lipids that have not been explored before in the context of PD.

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“…An article confirmed the effect of serotonin (5-hydroxytryptamine [5-HT]) deficiency on swallowing function [ 46 ]. In VFSS analysis, 5-HT deficiency had an impact on all three phases of swallowing.…”

Section: Resultsmentioning

confidence: 99%

“…Increased risk in aspiration was reported in rats with experimentally induced pulmonary emphysema and pulmonary fibrosis [ 43 , 44 ]. Additionally, probability of dysphagia was also identified in Rdh10 mutant mice with cleft palate due to retinoid deficiency, TPH2 knockout (TPH -/- ) mice with serotonin (5-hydroxytryptamine [5-HT]) deficiency, and Uch-L1 gad /Uch-L3 Δ 3–7 double homozygous mice used as a neuro-degenerative animal model [ 45 , 46 , 47 ].…”

Section: Discussionmentioning

confidence: 99%

A Systematic Review of Oropharyngeal Dysphagia Models in Rodents

Kim

2021

IJERPH

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Oropharyngeal dysphagia is a condition characterized by swallowing difficulty in the mouth and pharynx, which can be due to various factors. Animal models of oropharyngeal dysphagia are essential to confirm the cause-specific symptoms, pathological findings, and the effect of treatment. Recently, various animal models of dysphagia have been reported. The purpose of this review is to organize the rodent models of oropharyngeal dysphagia reported to date. The articles were obtained from Medline, Embase, and the Cochrane library, and selected following the PRISMA guideline. The animal models in which oropharyngeal dysphagia was induced in rats or mice were selected and classified based on the diseases causing oropharyngeal dysphagia. The animal used, method of inducing dysphagia, and screening methods and results were collected from the selected 37 articles. Various rodent models of oropharyngeal dysphagia provide distinctive information on atypical swallowing. Applying and analyzing the treatment in rodent models of dysphagia induced from various causes is an essential process to develop symptom-specific treatments. Therefore, the results of this study provide fundamental and important data for selecting appropriate animal models to study dysphagia.

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Mice Lacking Brain‐Derived Serotonin Have Altered Swallowing Function

Cited by 19 publications

References 23 publications

Quipazine Elicits Swallowing in the Arterially Perfused Rat Preparation: A Role for Medullary Raphe Nuclei?

Quipazine Elicits Swallowing in the Arterially Perfused Rat Preparation: A Role for Medullary Raphe Nuclei?

Explorative Combined Lipid and Transcriptomic Profiling of Substantia Nigra and Putamen in Parkinson’s Disease

A Systematic Review of Oropharyngeal Dysphagia Models in Rodents

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