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Mutant huntingtin expression in somatostatin-positive interneurons contributes to neurophysiological and behavioral phenotypes in BACHD mice.

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Title: Mutant huntingtin expression in somatostatin-positive interneurons contributes to neurophysiological and behavioral phenotypes in BACHD mice.
Authors: Fowler JA; Department of Neurology, Killion Center for Neurodegeneration and Experimental Therapeutics, The University of Alabama at Birmingham Heersink School of Medicine, Birmingham, AL 35294, USA.; Graduate Biomedical Sciences, Biochemistry and Structural Biology Theme, The University of Alabama at Birmingham Heersink School of Medicine, Birmingham, AL 35294, USA., Scarduzio M; Department of Neurology, Killion Center for Neurodegeneration and Experimental Therapeutics, The University of Alabama at Birmingham Heersink School of Medicine, Birmingham, AL 35294, USA., Pool C; College of Arts and Sciences, Xavier University of Louisiana, New Orleans, LA 70125, USA.; Summer in Biomedical Sciences (SIBS) Undergraduate Research Program, The University of Alabama at Birmingham, Birmingham, AL 35294, USA., Mahan CD; Department of Neurology, Killion Center for Neurodegeneration and Experimental Therapeutics, The University of Alabama at Birmingham Heersink School of Medicine, Birmingham, AL 35294, USA., Gray M; Department of Neurology, Killion Center for Neurodegeneration and Experimental Therapeutics, The University of Alabama at Birmingham Heersink School of Medicine, Birmingham, AL 35294, USA.
Source: Disease models & mechanisms [Dis Model Mech] 2026 Mar 01; Vol. 19 (3). Date of Electronic Publication: 2026 Mar 27.
Publication Type: Journal Article
Language: English
Journal Info: Publisher: Company of Biologists Ltd Country of Publication: England NLM ID: 101483332 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1754-8411 (Electronic) Linking ISSN: 17548403 NLM ISO Abbreviation: Dis Model Mech Subsets: MEDLINE
Imprint Name(s): Original Publication: Cambridge : Company of Biologists Ltd., c2008-
MeSH Terms: Interneurons*/metabolism , Huntingtin Protein*/metabolism , Huntingtin Protein*/genetics , Somatostatin*/metabolism , Mutation*/genetics , Mutant Proteins*/metabolism , Behavior, Animal*, Anxiety/physiopathology ; Anxiety/complications ; Huntington Disease/physiopathology ; Animals ; Phenotype ; Male ; Motor Activity ; Mice
Abstract: Huntington's disease (HD) is caused by expansion of the polyglutamine stretch in the widely expressed huntingtin (HTT) protein. Patients with HD have motor, psychiatric and cognitive changes due to changes in a variety of neural circuits. Somatostatin-expressing interneurons (SST-INs) can regulate neural circuits largely by inhibiting their target cells. Behaviorally, brain-wide inhibition of SST-INs increased anxiety in mice. Silencing striatal SST-INs caused a decrease in movement in the open field. Mutant HTT (mHTT)-expressing mice exhibited abnormal motor, cognitive and psychiatric-like changes, as well as electrophysiological changes in a variety of neurons, including striatal SST-INs. However, it is unknown whether cell-autonomous expression of mHTT in SST-INs contributes to HD-associated behavioral phenotypes or causes abnormal electrophysiological changes in striatal SST-INs. To address these questions, we reduced mHTT expression in SST-INs throughout the brain of BACHD mice. Our findings show that brain-wide reduction of mHTT in SST-INs rescues anxiety-like behavior in male BACHD mice in the light-dark box, without improving performance in the open field or on the rotarod. Additionally, expression of mHTT in striatal SST-INs cell autonomously drives their increased excitability.
(© 2026. Published by The Company of Biologists.)
Competing Interests: Competing interests The authors declare no competing or financial interests.
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Grant Information: 5R01NS089750 United States NS NINDS NIH HHS; Jarman F. Lowder Endowment; Hereditary Disease Foundation; University of Alabama at Birmingham
Contributed Indexing: Keywords: BACHD; Huntington's disease; Interneurons; Somatostatin; Striatum
Substance Nomenclature: 0 (Huntingtin Protein)
51110-01-1 (Somatostatin)
0 (Mutant Proteins)
Entry Date(s): Date Created: 20260206 Date Completed: 20260707 Latest Revision: 20260813
Update Code: 20260813
PubMed Central ID: PMC13054931
DOI: 10.1242/dmm.052513
PMID: 41648922
Database: MEDLINE
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  Data: Mutant huntingtin expression in somatostatin-positive interneurons contributes to neurophysiological and behavioral phenotypes in BACHD mice.
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  Data: <searchLink fieldCode="AU" term="%22Fowler+JA%22">Fowler JA</searchLink>; Department of Neurology, Killion Center for Neurodegeneration and Experimental Therapeutics, The University of Alabama at Birmingham Heersink School of Medicine, Birmingham, AL 35294, USA.; Graduate Biomedical Sciences, Biochemistry and Structural Biology Theme, The University of Alabama at Birmingham Heersink School of Medicine, Birmingham, AL 35294, USA.<br /><searchLink fieldCode="AU" term="%22Scarduzio+M%22">Scarduzio M</searchLink>; Department of Neurology, Killion Center for Neurodegeneration and Experimental Therapeutics, The University of Alabama at Birmingham Heersink School of Medicine, Birmingham, AL 35294, USA.<br /><searchLink fieldCode="AU" term="%22Pool+C%22">Pool C</searchLink>; College of Arts and Sciences, Xavier University of Louisiana, New Orleans, LA 70125, USA.; Summer in Biomedical Sciences (SIBS) Undergraduate Research Program, The University of Alabama at Birmingham, Birmingham, AL 35294, USA.<br /><searchLink fieldCode="AU" term="%22Mahan+CD%22">Mahan CD</searchLink>; Department of Neurology, Killion Center for Neurodegeneration and Experimental Therapeutics, The University of Alabama at Birmingham Heersink School of Medicine, Birmingham, AL 35294, USA.<br /><searchLink fieldCode="AU" term="%22Gray+M%22">Gray M</searchLink>; Department of Neurology, Killion Center for Neurodegeneration and Experimental Therapeutics, The University of Alabama at Birmingham Heersink School of Medicine, Birmingham, AL 35294, USA.
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  Data: <searchLink fieldCode="JN" term="%22101483332%22">Disease models & mechanisms</searchLink> [Dis Model Mech] 2026 Mar 01; Vol. 19 (3). <i>Date of Electronic Publication: </i>2026 Mar 27.
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  Data: <i>Original Publication</i>: Cambridge : Company of Biologists Ltd., c2008-
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  Data: <searchLink fieldCode="MM" term="%22Interneurons%22">Interneurons*</searchLink>/<searchLink fieldCode="MM" term="%22Interneurons+metabolism%22">metabolism</searchLink> <br /><searchLink fieldCode="MM" term="%22Huntingtin+Protein%22">Huntingtin Protein*</searchLink>/<searchLink fieldCode="MM" term="%22Huntingtin+Protein+metabolism%22">metabolism</searchLink> <br /><searchLink fieldCode="MM" term="%22Huntingtin+Protein%22">Huntingtin Protein*</searchLink>/<searchLink fieldCode="MM" term="%22Huntingtin+Protein+genetics%22">genetics</searchLink> <br /><searchLink fieldCode="MM" term="%22Somatostatin%22">Somatostatin*</searchLink>/<searchLink fieldCode="MM" term="%22Somatostatin+metabolism%22">metabolism</searchLink> <br /><searchLink fieldCode="MM" term="%22Mutation%22">Mutation*</searchLink>/<searchLink fieldCode="MM" term="%22Mutation+genetics%22">genetics</searchLink> <br /><searchLink fieldCode="MM" term="%22Mutant+Proteins%22">Mutant Proteins*</searchLink>/<searchLink fieldCode="MM" term="%22Mutant+Proteins+metabolism%22">metabolism</searchLink> <br /><searchLink fieldCode="MM" term="%22Behavior%2C+Animal%22">Behavior, Animal*</searchLink><br /><searchLink fieldCode="MH" term="%22Anxiety%22">Anxiety</searchLink>/<searchLink fieldCode="MH" term="%22Anxiety+physiopathology%22">physiopathology</searchLink> ; <searchLink fieldCode="MH" term="%22Anxiety%22">Anxiety</searchLink>/<searchLink fieldCode="MH" term="%22Anxiety+complications%22">complications</searchLink> ; <searchLink fieldCode="MH" term="%22Huntington+Disease%22">Huntington Disease</searchLink>/<searchLink fieldCode="MH" term="%22Huntington+Disease+physiopathology%22">physiopathology</searchLink> ; <searchLink fieldCode="MH" term="%22Animals%22">Animals</searchLink> ; <searchLink fieldCode="MH" term="%22Phenotype%22">Phenotype</searchLink> ; <searchLink fieldCode="MH" term="%22Male%22">Male</searchLink> ; <searchLink fieldCode="MH" term="%22Motor+Activity%22">Motor Activity</searchLink> ; <searchLink fieldCode="MH" term="%22Mice%22">Mice</searchLink>
– Name: Abstract
  Label: Abstract
  Group: Ab
  Data: Huntington's disease (HD) is caused by expansion of the polyglutamine stretch in the widely expressed huntingtin (HTT) protein. Patients with HD have motor, psychiatric and cognitive changes due to changes in a variety of neural circuits. Somatostatin-expressing interneurons (SST-INs) can regulate neural circuits largely by inhibiting their target cells. Behaviorally, brain-wide inhibition of SST-INs increased anxiety in mice. Silencing striatal SST-INs caused a decrease in movement in the open field. Mutant HTT (mHTT)-expressing mice exhibited abnormal motor, cognitive and psychiatric-like changes, as well as electrophysiological changes in a variety of neurons, including striatal SST-INs. However, it is unknown whether cell-autonomous expression of mHTT in SST-INs contributes to HD-associated behavioral phenotypes or causes abnormal electrophysiological changes in striatal SST-INs. To address these questions, we reduced mHTT expression in SST-INs throughout the brain of BACHD mice. Our findings show that brain-wide reduction of mHTT in SST-INs rescues anxiety-like behavior in male BACHD mice in the light-dark box, without improving performance in the open field or on the rotarod. Additionally, expression of mHTT in striatal SST-INs cell autonomously drives their increased excitability.<br /> (© 2026. Published by The Company of Biologists.)
– Name: Abstract
  Label: Competing Interests
  Group: Ab
  Data: Competing interests The authors declare no competing or financial interests.
– Name: Ref
  Label: References
  Group: RefInfo
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– Name: GrantInfo
  Label: Grant Information
  Group: Grant
  Data: 5R01NS089750 United States NS NINDS NIH HHS; Jarman F. Lowder Endowment; Hereditary Disease Foundation; University of Alabama at Birmingham
– Name: SubjectMinor
  Label: Contributed Indexing
  Group:
  Data: <i>Keywords: </i>BACHD; Huntington's disease; Interneurons; Somatostatin; Striatum
– Name: NumberCAS
  Label: Substance Nomenclature
  Group: ID
  Data: 0 (Huntingtin Protein)<br />51110-01-1 (Somatostatin)<br />0 (Mutant Proteins)
– Name: DateEntry
  Label: Entry Date(s)
  Group: Date
  Data: <i>Date Created: </i>20260206 <i>Date Completed: </i>20260707 <i>Latest Revision: </i>20260813
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  Label: Update Code
  Group: Date
  Data: 20260813
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  Label: PubMed Central ID
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  Data: PMC13054931
– Name: DOI
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  Group: ID
  Data: 10.1242/dmm.052513
– Name: AN
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PLink https://search.ebscohost.com/login.aspx?direct=true&site=eds-live&db=cmedm&AN=41648922
RecordInfo BibRecord:
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      – Type: doi
        Value: 10.1242/dmm.052513
    Languages:
      – Code: eng
        Text: English
    Subjects:
      – SubjectFull: Anxiety physiopathology
        Type: general
      – SubjectFull: Anxiety complications
        Type: general
      – SubjectFull: Huntington Disease physiopathology
        Type: general
      – SubjectFull: Animals
        Type: general
      – SubjectFull: Phenotype
        Type: general
      – SubjectFull: Male
        Type: general
      – SubjectFull: Motor Activity
        Type: general
      – SubjectFull: Mice
        Type: general
      – SubjectFull: Interneurons metabolism
        Type: general
      – SubjectFull: Huntingtin Protein metabolism
        Type: general
      – SubjectFull: Huntingtin Protein genetics
        Type: general
      – SubjectFull: Somatostatin metabolism
        Type: general
      – SubjectFull: Mutation genetics
        Type: general
      – SubjectFull: Mutant Proteins metabolism
        Type: general
      – SubjectFull: Behavior, Animal
        Type: general
    Titles:
      – TitleFull: Mutant huntingtin expression in somatostatin-positive interneurons contributes to neurophysiological and behavioral phenotypes in BACHD mice.
        Type: main
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            NameFull: Fowler JA
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          Dates:
            – D: 01
              M: 03
              Text: 2026 Mar 01
              Type: published
              Y: 2026
          Identifiers:
            – Type: issn-electronic
              Value: 1754-8411
          Numbering:
            – Type: volume
              Value: 19
            – Type: issue
              Value: 3
          Titles:
            – TitleFull: Disease models & mechanisms
              Type: main
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