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FOXP2 Expression in Rodent, Rhesus Monkey, and Human Brainstem.

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Title: FOXP2 Expression in Rodent, Rhesus Monkey, and Human Brainstem.
Authors: Vallin, Eric1, Mostaert, Brian1, Thayer, Emma1, Cho, Hyunjin1,2, Hoffman, Matthew R.1, Cassell, Martin1, Van Daele, Douglas1 douglas-van-daele@uiowa.edu
Source: Journal of Speech, Language & Hearing Research. Sep2025, Vol. 68 Issue 9, p4177-4187. 11p.
Subject Terms: *Qualitative research, *Research methodology, *Speech disorders, *Comparative studies, Protein metabolism, Rodents, Biological models, Research funding, Cluster analysis (Statistics), Transcription factors, Descriptive statistics, Gene expression, Immunohistochemistry, Apraxia, Brain stem, Animal experimentation, Data analysis software, Primates
Abstract: Background: The FOXP2 gene encodes a transcription factor responsible for the development of neural structures involved in vocalization in vertebrates. Animal models have proven critical in the study of FOXP2 gene expression, although a comparative interspecies analysis of brainstem structures is understudied. This study evaluates the expression of FOXP2 protein within the brainstem of rats, rhesus monkeys, and humans. Method: Brainstems of one rat, two rhesus monkeys, and one human were harvested. Immunohistochemistry for FOXP2 was performed, followed by imaging and centroid analysis to identify patterns of expression within the brainstems of the three species. Images were examined with a Nikon Eclipse 80i microscope (Nikon Corporation) in conjunction with Neurolucida software (Version 8; MBF Bioscience) to capture FOXP2 protein in the three-dimensional brainstem landscape in monkeys and rodents. The 50-μm slices chosen for centroid analysis contained the dorsolateral pons and the dorsal medulla, areas that may play a role in FOXP2-related oromotor dyspraxia. Results: Similarities were observed in the pattern of FOXP2-positive cells and centroids across species, showing a wide distribution of centroids rostrally and medial convergence of centroids caudally. This pattern exhibited rostrolateral-to-caudomedial tapering in both the pons and the medulla. Neural structures crucial for speech exhibited strong FOXP2 staining, including the gigantocellular, parvocellular, and intermediate medullary reticular nuclei, as well as the medullary respiratory columns, the NTS, and the Bötzinger and preBötzinger complexes. Conclusions: Respiratory pattern generators in the dorsolateral pons and medulla, which house critical premotor neurons for language generation, show similar FOXP2 protein expression across the rat, rhesus monkey, and human. As FOXP2 protein expression is conserved across multiple species, animal models may be valuable resources in studying FOXP2-related disorders, including dyspraxia. [ABSTRACT FROM AUTHOR]
Copyright of Journal of Speech, Language & Hearing Research is the property of American Speech-Language-Hearing Association and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
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  Data: FOXP2 Expression in Rodent, Rhesus Monkey, and Human Brainstem.
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  Data: <searchLink fieldCode="AR" term="%22Vallin%2C+Eric%22">Vallin, Eric</searchLink><relatesTo>1</relatesTo><br /><searchLink fieldCode="AR" term="%22Mostaert%2C+Brian%22">Mostaert, Brian</searchLink><relatesTo>1</relatesTo><br /><searchLink fieldCode="AR" term="%22Thayer%2C+Emma%22">Thayer, Emma</searchLink><relatesTo>1</relatesTo><br /><searchLink fieldCode="AR" term="%22Cho%2C+Hyunjin%22">Cho, Hyunjin</searchLink><relatesTo>1,2</relatesTo><br /><searchLink fieldCode="AR" term="%22Hoffman%2C+Matthew+R%2E%22">Hoffman, Matthew R.</searchLink><relatesTo>1</relatesTo><br /><searchLink fieldCode="AR" term="%22Cassell%2C+Martin%22">Cassell, Martin</searchLink><relatesTo>1</relatesTo><br /><searchLink fieldCode="AR" term="%22Van+Daele%2C+Douglas%22">Van Daele, Douglas</searchLink><relatesTo>1</relatesTo><i> douglas-van-daele@uiowa.edu</i>
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  Data: <searchLink fieldCode="JN" term="%22Journal+of+Speech%2C+Language+%26+Hearing+Research%22">Journal of Speech, Language & Hearing Research</searchLink>. Sep2025, Vol. 68 Issue 9, p4177-4187. 11p.
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  Data: *<searchLink fieldCode="DE" term="%22Qualitative+research%22">Qualitative research</searchLink><br />*<searchLink fieldCode="DE" term="%22Research+methodology%22">Research methodology</searchLink><br />*<searchLink fieldCode="DE" term="%22Speech+disorders%22">Speech disorders</searchLink><br />*<searchLink fieldCode="DE" term="%22Comparative+studies%22">Comparative studies</searchLink><br /><searchLink fieldCode="DE" term="%22Protein+metabolism%22">Protein metabolism</searchLink><br /><searchLink fieldCode="DE" term="%22Rodents%22">Rodents</searchLink><br /><searchLink fieldCode="DE" term="%22Biological+models%22">Biological models</searchLink><br /><searchLink fieldCode="DE" term="%22Research+funding%22">Research funding</searchLink><br /><searchLink fieldCode="DE" term="%22Cluster+analysis+%28Statistics%29%22">Cluster analysis (Statistics)</searchLink><br /><searchLink fieldCode="DE" term="%22Transcription+factors%22">Transcription factors</searchLink><br /><searchLink fieldCode="DE" term="%22Descriptive+statistics%22">Descriptive statistics</searchLink><br /><searchLink fieldCode="DE" term="%22Gene+expression%22">Gene expression</searchLink><br /><searchLink fieldCode="DE" term="%22Immunohistochemistry%22">Immunohistochemistry</searchLink><br /><searchLink fieldCode="DE" term="%22Apraxia%22">Apraxia</searchLink><br /><searchLink fieldCode="DE" term="%22Brain+stem%22">Brain stem</searchLink><br /><searchLink fieldCode="DE" term="%22Animal+experimentation%22">Animal experimentation</searchLink><br /><searchLink fieldCode="DE" term="%22Data+analysis+software%22">Data analysis software</searchLink><br /><searchLink fieldCode="DE" term="%22Primates%22">Primates</searchLink>
– Name: Abstract
  Label: Abstract
  Group: Ab
  Data: Background: The FOXP2 gene encodes a transcription factor responsible for the development of neural structures involved in vocalization in vertebrates. Animal models have proven critical in the study of FOXP2 gene expression, although a comparative interspecies analysis of brainstem structures is understudied. This study evaluates the expression of FOXP2 protein within the brainstem of rats, rhesus monkeys, and humans. Method: Brainstems of one rat, two rhesus monkeys, and one human were harvested. Immunohistochemistry for FOXP2 was performed, followed by imaging and centroid analysis to identify patterns of expression within the brainstems of the three species. Images were examined with a Nikon Eclipse 80i microscope (Nikon Corporation) in conjunction with Neurolucida software (Version 8; MBF Bioscience) to capture FOXP2 protein in the three-dimensional brainstem landscape in monkeys and rodents. The 50-μm slices chosen for centroid analysis contained the dorsolateral pons and the dorsal medulla, areas that may play a role in FOXP2-related oromotor dyspraxia. Results: Similarities were observed in the pattern of FOXP2-positive cells and centroids across species, showing a wide distribution of centroids rostrally and medial convergence of centroids caudally. This pattern exhibited rostrolateral-to-caudomedial tapering in both the pons and the medulla. Neural structures crucial for speech exhibited strong FOXP2 staining, including the gigantocellular, parvocellular, and intermediate medullary reticular nuclei, as well as the medullary respiratory columns, the NTS, and the Bötzinger and preBötzinger complexes. Conclusions: Respiratory pattern generators in the dorsolateral pons and medulla, which house critical premotor neurons for language generation, show similar FOXP2 protein expression across the rat, rhesus monkey, and human. As FOXP2 protein expression is conserved across multiple species, animal models may be valuable resources in studying FOXP2-related disorders, including dyspraxia. [ABSTRACT FROM AUTHOR]
– Name: AbstractSuppliedCopyright
  Label:
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  Data: <i>Copyright of Journal of Speech, Language & Hearing Research is the property of American Speech-Language-Hearing Association and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract.</i> (Copyright applies to all Abstracts.)
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RecordInfo BibRecord:
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      – Type: doi
        Value: 10.1044/2025_JSLHR-24-00332
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      – Code: eng
        Text: English
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      Pagination:
        PageCount: 11
        StartPage: 4177
    Subjects:
      – SubjectFull: Qualitative research
        Type: general
      – SubjectFull: Research methodology
        Type: general
      – SubjectFull: Speech disorders
        Type: general
      – SubjectFull: Comparative studies
        Type: general
      – SubjectFull: Protein metabolism
        Type: general
      – SubjectFull: Rodents
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      – SubjectFull: Biological models
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      – SubjectFull: Research funding
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      – SubjectFull: Transcription factors
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      – SubjectFull: Descriptive statistics
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      – SubjectFull: Gene expression
        Type: general
      – SubjectFull: Immunohistochemistry
        Type: general
      – SubjectFull: Apraxia
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      – SubjectFull: Brain stem
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      – SubjectFull: Animal experimentation
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      – SubjectFull: Data analysis software
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      – SubjectFull: Primates
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      – TitleFull: FOXP2 Expression in Rodent, Rhesus Monkey, and Human Brainstem.
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              M: 09
              Text: Sep2025
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              Y: 2025
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