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No Gastrointestinal Dysmotility in Transgenic Mouse Models of Migraine
Author(s) -
Sprouse Blum Adam S.,
Lavoie Brigitte,
Haag Melody,
Mawe Seamus M.,
Tolner Else A.,
Maagdenberg Arn M.J.M.,
Chen ShihPin,
EikermannHaerter Katharina,
Ptáček Louis,
Mawe Gary M.,
Shapiro Robert E.
Publication year - 2020
Publication title -
headache: the journal of head and face pain
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.14
H-Index - 119
eISSN - 1526-4610
pISSN - 0017-8748
DOI - 10.1111/head.13724
Subject(s) - migraine , motility , gastric emptying , phenotype , medicine , genetically modified mouse , gastroenterology , biology , transgene , stomach , gene , genetics
Objective To determine whether transgenic mouse models of migraine exhibit upper gastrointestinal dysmotility comparable to those observed in migraine patients. Background There is considerable evidence supporting the comorbidity of gastrointestinal dysmotility and migraine. Gastrointestinal motility, however, has never been investigated in transgenic mouse models of migraine. Methods Three transgenic mouse strains that express pathogenic gene mutations linked to monogenic migraine‐relevant phenotypes were studied: CADASIL ( Notch3 ‐Tg88), FASP ( CSNK1D ‐T44A), and FHM1 ( CACNA1A ‐S218L). Upper gastrointestinal motility was quantified by measuring gastric emptying and small intestinal transit in mutant and control animals. Gastrointestinal motility was measured at baseline and after pretreatment with 10 mg/kg nitroglycerin (NTG). Results No significant differences were observed for gastric emptying or small intestinal transit at baseline for any of the 3 transgenic strains when compared to appropriate controls or after pretreatment with NTG when compared to vehicle. Conclusions We detected no evidence of upper gastrointestinal dysmotility in mice that express mutations in genes linked to monogenic migraine‐relevant phenotypes. Future studies seeking to understand why humans with migraine experience delayed gastric emptying may benefit from pursuing other modifiers of gastrointestinal motility, such as epigenetic or microbiome‐related factors.