Huntington mice demonstrate diminished pain response in inflammatory pain model

Ya Chi Lin, Hung Tsung Hsiao, Sheng-Nan Wu, Yen-Chin Liu

Research output: Contribution to journalArticle

3 Citations (Scopus)

Abstract

BACKGROUND: Huntington disease (HD) affects the nervous system and leads to mental and motor dysfunction. Previous studies have shown that HD is caused by the exon 1 region of the huntingtin (HTT) gene having expanded CAG trinucleotide repeats. However, few studies have focused on the relationship between HD and pain. The purpose of this study is to investigate the relationship between HD and pain response. METHODS: We used clinical similar transgenic HD mice carrying a mutant HTT exon 1 containing 84 CAG trinucleotide repeats to evaluate the relationship between HD and pain. Inflammatory pain models were induced by either formalin or complete Freund adjuvant injection over the hind paw. Spinal cord, dorsal root ganglion, and paw skin tissues were harvested at the end of the behavioral inflammatory pain studies. Immunofluorescence assay, Western blotting, and enzyme-linked immunosorbent assay were used to identify changes in cells and cytokines. RESULTS: Our data demonstrate that preonset HD mice exhibited less pain behavior than wild-type (WT) mice in both young (n = 11 [WT], 13 [HD]) and aged (n = 8 [WT], 9 [HD]) mice. Western blotting and immunohistological examination of lumbar spinal cord tissue and dorsal root ganglion indicate less activation of glial cells and astrocytes in young HD mice (n = 6–7) compared to that in WT mice (n = 6–7). The production levels of tumor necrosis factor-α, interleukin-1β, and substance P were also lower in young HD mice (n = 6–7). CONCLUSIONS: Our data demonstrate less pain behavior and pain-related cytokine response at the spinal cord level for HD mice compared to those for WT mice. Further studies are needed for determining the mechanism as to how mutant HTT leads to altered pain behavior and pain-related cytokine response.

Original languageEnglish
Pages (from-to)661-669
Number of pages9
JournalAnesthesia and analgesia
Volume126
Issue number2
DOIs
Publication statusPublished - 2018 Jan 1

Fingerprint

Huntington Disease
Pain
Spinal Cord
Spinal Ganglia
Cytokines
Exons
Western Blotting
Trinucleotide Repeat Expansion
Trinucleotide Repeats
Freund's Adjuvant
Substance P
Interleukin-1
Neuroglia
Astrocytes
Nervous System
Formaldehyde
Fluorescent Antibody Technique
Tumor Necrosis Factor-alpha
Enzyme-Linked Immunosorbent Assay

All Science Journal Classification (ASJC) codes

  • Anesthesiology and Pain Medicine

Cite this

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title = "Huntington mice demonstrate diminished pain response in inflammatory pain model",
abstract = "BACKGROUND: Huntington disease (HD) affects the nervous system and leads to mental and motor dysfunction. Previous studies have shown that HD is caused by the exon 1 region of the huntingtin (HTT) gene having expanded CAG trinucleotide repeats. However, few studies have focused on the relationship between HD and pain. The purpose of this study is to investigate the relationship between HD and pain response. METHODS: We used clinical similar transgenic HD mice carrying a mutant HTT exon 1 containing 84 CAG trinucleotide repeats to evaluate the relationship between HD and pain. Inflammatory pain models were induced by either formalin or complete Freund adjuvant injection over the hind paw. Spinal cord, dorsal root ganglion, and paw skin tissues were harvested at the end of the behavioral inflammatory pain studies. Immunofluorescence assay, Western blotting, and enzyme-linked immunosorbent assay were used to identify changes in cells and cytokines. RESULTS: Our data demonstrate that preonset HD mice exhibited less pain behavior than wild-type (WT) mice in both young (n = 11 [WT], 13 [HD]) and aged (n = 8 [WT], 9 [HD]) mice. Western blotting and immunohistological examination of lumbar spinal cord tissue and dorsal root ganglion indicate less activation of glial cells and astrocytes in young HD mice (n = 6–7) compared to that in WT mice (n = 6–7). The production levels of tumor necrosis factor-α, interleukin-1β, and substance P were also lower in young HD mice (n = 6–7). CONCLUSIONS: Our data demonstrate less pain behavior and pain-related cytokine response at the spinal cord level for HD mice compared to those for WT mice. Further studies are needed for determining the mechanism as to how mutant HTT leads to altered pain behavior and pain-related cytokine response.",
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Huntington mice demonstrate diminished pain response in inflammatory pain model. / Lin, Ya Chi; Hsiao, Hung Tsung; Wu, Sheng-Nan; Liu, Yen-Chin.

In: Anesthesia and analgesia, Vol. 126, No. 2, 01.01.2018, p. 661-669.

Research output: Contribution to journalArticle

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AU - Lin, Ya Chi

AU - Hsiao, Hung Tsung

AU - Wu, Sheng-Nan

AU - Liu, Yen-Chin

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N2 - BACKGROUND: Huntington disease (HD) affects the nervous system and leads to mental and motor dysfunction. Previous studies have shown that HD is caused by the exon 1 region of the huntingtin (HTT) gene having expanded CAG trinucleotide repeats. However, few studies have focused on the relationship between HD and pain. The purpose of this study is to investigate the relationship between HD and pain response. METHODS: We used clinical similar transgenic HD mice carrying a mutant HTT exon 1 containing 84 CAG trinucleotide repeats to evaluate the relationship between HD and pain. Inflammatory pain models were induced by either formalin or complete Freund adjuvant injection over the hind paw. Spinal cord, dorsal root ganglion, and paw skin tissues were harvested at the end of the behavioral inflammatory pain studies. Immunofluorescence assay, Western blotting, and enzyme-linked immunosorbent assay were used to identify changes in cells and cytokines. RESULTS: Our data demonstrate that preonset HD mice exhibited less pain behavior than wild-type (WT) mice in both young (n = 11 [WT], 13 [HD]) and aged (n = 8 [WT], 9 [HD]) mice. Western blotting and immunohistological examination of lumbar spinal cord tissue and dorsal root ganglion indicate less activation of glial cells and astrocytes in young HD mice (n = 6–7) compared to that in WT mice (n = 6–7). The production levels of tumor necrosis factor-α, interleukin-1β, and substance P were also lower in young HD mice (n = 6–7). CONCLUSIONS: Our data demonstrate less pain behavior and pain-related cytokine response at the spinal cord level for HD mice compared to those for WT mice. Further studies are needed for determining the mechanism as to how mutant HTT leads to altered pain behavior and pain-related cytokine response.

AB - BACKGROUND: Huntington disease (HD) affects the nervous system and leads to mental and motor dysfunction. Previous studies have shown that HD is caused by the exon 1 region of the huntingtin (HTT) gene having expanded CAG trinucleotide repeats. However, few studies have focused on the relationship between HD and pain. The purpose of this study is to investigate the relationship between HD and pain response. METHODS: We used clinical similar transgenic HD mice carrying a mutant HTT exon 1 containing 84 CAG trinucleotide repeats to evaluate the relationship between HD and pain. Inflammatory pain models were induced by either formalin or complete Freund adjuvant injection over the hind paw. Spinal cord, dorsal root ganglion, and paw skin tissues were harvested at the end of the behavioral inflammatory pain studies. Immunofluorescence assay, Western blotting, and enzyme-linked immunosorbent assay were used to identify changes in cells and cytokines. RESULTS: Our data demonstrate that preonset HD mice exhibited less pain behavior than wild-type (WT) mice in both young (n = 11 [WT], 13 [HD]) and aged (n = 8 [WT], 9 [HD]) mice. Western blotting and immunohistological examination of lumbar spinal cord tissue and dorsal root ganglion indicate less activation of glial cells and astrocytes in young HD mice (n = 6–7) compared to that in WT mice (n = 6–7). The production levels of tumor necrosis factor-α, interleukin-1β, and substance P were also lower in young HD mice (n = 6–7). CONCLUSIONS: Our data demonstrate less pain behavior and pain-related cytokine response at the spinal cord level for HD mice compared to those for WT mice. Further studies are needed for determining the mechanism as to how mutant HTT leads to altered pain behavior and pain-related cytokine response.

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