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Histamine Modulation of Acute Nociception Involves Regulation of Nav1.8 in Primary Afferent Neurons in Mice
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| Zeitschriftentitel: | CNS Neuroscience & Therapeutics |
|---|---|
| Personen und Körperschaften: | , , , , , , , , , , |
| In: | CNS Neuroscience & Therapeutics, 19, 2013, 9, S. 649-658 |
| Format: | E-Article |
| Sprache: | Englisch |
| veröffentlicht: |
Wiley
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| Schlagwörter: |
| author_facet |
Yu, Jie Fang, Qi Lou, Guo‐Dong Shou, Wen‐Ting Yue, Jia‐Xing Tang, Ying‐Ying Hou, Wei‐Wei Xu, Tian‐Le Ohtsu, Hiroshi Zhang, Shi‐Hong Chen, Zhong Yu, Jie Fang, Qi Lou, Guo‐Dong Shou, Wen‐Ting Yue, Jia‐Xing Tang, Ying‐Ying Hou, Wei‐Wei Xu, Tian‐Le Ohtsu, Hiroshi Zhang, Shi‐Hong Chen, Zhong |
|---|---|
| author |
Yu, Jie Fang, Qi Lou, Guo‐Dong Shou, Wen‐Ting Yue, Jia‐Xing Tang, Ying‐Ying Hou, Wei‐Wei Xu, Tian‐Le Ohtsu, Hiroshi Zhang, Shi‐Hong Chen, Zhong |
| spellingShingle |
Yu, Jie Fang, Qi Lou, Guo‐Dong Shou, Wen‐Ting Yue, Jia‐Xing Tang, Ying‐Ying Hou, Wei‐Wei Xu, Tian‐Le Ohtsu, Hiroshi Zhang, Shi‐Hong Chen, Zhong CNS Neuroscience & Therapeutics Histamine Modulation of Acute Nociception Involves Regulation of Nav1.8 in Primary Afferent Neurons in Mice Pharmacology (medical) Physiology (medical) Psychiatry and Mental health Pharmacology |
| author_sort |
yu, jie |
| spelling |
Yu, Jie Fang, Qi Lou, Guo‐Dong Shou, Wen‐Ting Yue, Jia‐Xing Tang, Ying‐Ying Hou, Wei‐Wei Xu, Tian‐Le Ohtsu, Hiroshi Zhang, Shi‐Hong Chen, Zhong 1755-5930 1755-5949 Wiley Pharmacology (medical) Physiology (medical) Psychiatry and Mental health Pharmacology http://dx.doi.org/10.1111/cns.12134 <jats:title>Summary</jats:title><jats:sec><jats:title>Aims</jats:title><jats:p>To explore the role of histamine in acute pain perception and its possible mechanisms.</jats:p></jats:sec><jats:sec><jats:title>Methods</jats:title><jats:p>Pain‐like behaviors induced by four types of noxious stimuli (hot‐plate, tail‐pressure, acetic acid, and formalin) were accessed in mice. Na<jats:sub>v</jats:sub>1.8 expression and functions in primary afferent neurons were compared between histidine decarboxylase knockout (<jats:styled-content style="fixed-case">HDC</jats:styled-content><jats:sup>−/−</jats:sup>) mice and their wild‐types.</jats:p></jats:sec><jats:sec><jats:title>Results</jats:title><jats:p><jats:styled-content style="fixed-case">HDC</jats:styled-content><jats:sup>−/−</jats:sup> mice, lacking in endogenous histamine, showed elevated sensitivity to all these noxious stimuli, as compared with the wild‐types. In addition, a depletion of endogenous histamine with α‐fluoromethylhistidine (α‐<jats:styled-content style="fixed-case">FMH</jats:styled-content>), a specific <jats:styled-content style="fixed-case">HDC</jats:styled-content> inhibitor, or feeding mice a low‐histamine diet also enhanced nociception in the wild‐types. Na<jats:sub>v</jats:sub>1.8 expression in primary afferent neurons was increased both in <jats:styled-content style="fixed-case">HDC</jats:styled-content><jats:sup>−/−</jats:sup> and in α‐<jats:styled-content style="fixed-case">FMH</jats:styled-content>‐treated wild‐type mice. A higher Na<jats:sub>v</jats:sub>1.8 current density, a lower action potential (<jats:styled-content style="fixed-case">AP</jats:styled-content>) threshold, and a higher firing rate in response to suprathreshold stimulation were observed in nociception‐related small <jats:styled-content style="fixed-case">DRG</jats:styled-content> neurons of <jats:styled-content style="fixed-case">HDC</jats:styled-content><jats:sup>−/−</jats:sup> mice. Na<jats:sub>v</jats:sub>1.8 inhibitor A‐803467, but not <jats:styled-content style="fixed-case">TTX</jats:styled-content>, diminished the hyperexcitability and blocked repetitive <jats:styled-content style="fixed-case">AP</jats:styled-content> firing of these neurons.</jats:p></jats:sec><jats:sec><jats:title>Conclusion</jats:title><jats:p>Our results indicate that histamine participates in acute pain modulation in a dose‐related manner. The regulation of Na<jats:sub>v</jats:sub>1.8 expression and the excitability of nociceptive primary afferent neurons may be involved in the underlying mechanisms.</jats:p></jats:sec> Histamine Modulation of Acute Nociception Involves Regulation of Na<sub>v</sub>1.8 in Primary Afferent Neurons in Mice CNS Neuroscience & Therapeutics |
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10.1111/cns.12134 |
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Online Free |
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Chemie und Pharmazie Biologie Medizin Psychologie |
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Wiley, 2013 |
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Wiley, 2013 |
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1755-5930 1755-5949 |
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1755-5930 1755-5949 |
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yu2013histaminemodulationofacutenociceptioninvolvesregulationofnav18inprimaryafferentneuronsinmice |
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2013 |
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Wiley |
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CNS Neuroscience & Therapeutics |
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49 |
| title |
Histamine Modulation of Acute Nociception Involves Regulation of Nav1.8 in Primary Afferent Neurons in Mice |
| title_unstemmed |
Histamine Modulation of Acute Nociception Involves Regulation of Nav1.8 in Primary Afferent Neurons in Mice |
| title_full |
Histamine Modulation of Acute Nociception Involves Regulation of Nav1.8 in Primary Afferent Neurons in Mice |
| title_fullStr |
Histamine Modulation of Acute Nociception Involves Regulation of Nav1.8 in Primary Afferent Neurons in Mice |
| title_full_unstemmed |
Histamine Modulation of Acute Nociception Involves Regulation of Nav1.8 in Primary Afferent Neurons in Mice |
| title_short |
Histamine Modulation of Acute Nociception Involves Regulation of Nav1.8 in Primary Afferent Neurons in Mice |
| title_sort |
histamine modulation of acute nociception involves regulation of na<sub>v</sub>1.8 in primary afferent neurons in mice |
| topic |
Pharmacology (medical) Physiology (medical) Psychiatry and Mental health Pharmacology |
| url |
http://dx.doi.org/10.1111/cns.12134 |
| publishDate |
2013 |
| physical |
649-658 |
| description |
<jats:title>Summary</jats:title><jats:sec><jats:title>Aims</jats:title><jats:p>To explore the role of histamine in acute pain perception and its possible mechanisms.</jats:p></jats:sec><jats:sec><jats:title>Methods</jats:title><jats:p>Pain‐like behaviors induced by four types of noxious stimuli (hot‐plate, tail‐pressure, acetic acid, and formalin) were accessed in mice. Na<jats:sub>v</jats:sub>1.8 expression and functions in primary afferent neurons were compared between histidine decarboxylase knockout (<jats:styled-content style="fixed-case">HDC</jats:styled-content><jats:sup>−/−</jats:sup>) mice and their wild‐types.</jats:p></jats:sec><jats:sec><jats:title>Results</jats:title><jats:p><jats:styled-content style="fixed-case">HDC</jats:styled-content><jats:sup>−/−</jats:sup> mice, lacking in endogenous histamine, showed elevated sensitivity to all these noxious stimuli, as compared with the wild‐types. In addition, a depletion of endogenous histamine with α‐fluoromethylhistidine (α‐<jats:styled-content style="fixed-case">FMH</jats:styled-content>), a specific <jats:styled-content style="fixed-case">HDC</jats:styled-content> inhibitor, or feeding mice a low‐histamine diet also enhanced nociception in the wild‐types. Na<jats:sub>v</jats:sub>1.8 expression in primary afferent neurons was increased both in <jats:styled-content style="fixed-case">HDC</jats:styled-content><jats:sup>−/−</jats:sup> and in α‐<jats:styled-content style="fixed-case">FMH</jats:styled-content>‐treated wild‐type mice. A higher Na<jats:sub>v</jats:sub>1.8 current density, a lower action potential (<jats:styled-content style="fixed-case">AP</jats:styled-content>) threshold, and a higher firing rate in response to suprathreshold stimulation were observed in nociception‐related small <jats:styled-content style="fixed-case">DRG</jats:styled-content> neurons of <jats:styled-content style="fixed-case">HDC</jats:styled-content><jats:sup>−/−</jats:sup> mice. Na<jats:sub>v</jats:sub>1.8 inhibitor A‐803467, but not <jats:styled-content style="fixed-case">TTX</jats:styled-content>, diminished the hyperexcitability and blocked repetitive <jats:styled-content style="fixed-case">AP</jats:styled-content> firing of these neurons.</jats:p></jats:sec><jats:sec><jats:title>Conclusion</jats:title><jats:p>Our results indicate that histamine participates in acute pain modulation in a dose‐related manner. The regulation of Na<jats:sub>v</jats:sub>1.8 expression and the excitability of nociceptive primary afferent neurons may be involved in the underlying mechanisms.</jats:p></jats:sec> |
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| author | Yu, Jie, Fang, Qi, Lou, Guo‐Dong, Shou, Wen‐Ting, Yue, Jia‐Xing, Tang, Ying‐Ying, Hou, Wei‐Wei, Xu, Tian‐Le, Ohtsu, Hiroshi, Zhang, Shi‐Hong, Chen, Zhong |
| author_facet | Yu, Jie, Fang, Qi, Lou, Guo‐Dong, Shou, Wen‐Ting, Yue, Jia‐Xing, Tang, Ying‐Ying, Hou, Wei‐Wei, Xu, Tian‐Le, Ohtsu, Hiroshi, Zhang, Shi‐Hong, Chen, Zhong, Yu, Jie, Fang, Qi, Lou, Guo‐Dong, Shou, Wen‐Ting, Yue, Jia‐Xing, Tang, Ying‐Ying, Hou, Wei‐Wei, Xu, Tian‐Le, Ohtsu, Hiroshi, Zhang, Shi‐Hong, Chen, Zhong |
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| description | <jats:title>Summary</jats:title><jats:sec><jats:title>Aims</jats:title><jats:p>To explore the role of histamine in acute pain perception and its possible mechanisms.</jats:p></jats:sec><jats:sec><jats:title>Methods</jats:title><jats:p>Pain‐like behaviors induced by four types of noxious stimuli (hot‐plate, tail‐pressure, acetic acid, and formalin) were accessed in mice. Na<jats:sub>v</jats:sub>1.8 expression and functions in primary afferent neurons were compared between histidine decarboxylase knockout (<jats:styled-content style="fixed-case">HDC</jats:styled-content><jats:sup>−/−</jats:sup>) mice and their wild‐types.</jats:p></jats:sec><jats:sec><jats:title>Results</jats:title><jats:p><jats:styled-content style="fixed-case">HDC</jats:styled-content><jats:sup>−/−</jats:sup> mice, lacking in endogenous histamine, showed elevated sensitivity to all these noxious stimuli, as compared with the wild‐types. In addition, a depletion of endogenous histamine with α‐fluoromethylhistidine (α‐<jats:styled-content style="fixed-case">FMH</jats:styled-content>), a specific <jats:styled-content style="fixed-case">HDC</jats:styled-content> inhibitor, or feeding mice a low‐histamine diet also enhanced nociception in the wild‐types. Na<jats:sub>v</jats:sub>1.8 expression in primary afferent neurons was increased both in <jats:styled-content style="fixed-case">HDC</jats:styled-content><jats:sup>−/−</jats:sup> and in α‐<jats:styled-content style="fixed-case">FMH</jats:styled-content>‐treated wild‐type mice. A higher Na<jats:sub>v</jats:sub>1.8 current density, a lower action potential (<jats:styled-content style="fixed-case">AP</jats:styled-content>) threshold, and a higher firing rate in response to suprathreshold stimulation were observed in nociception‐related small <jats:styled-content style="fixed-case">DRG</jats:styled-content> neurons of <jats:styled-content style="fixed-case">HDC</jats:styled-content><jats:sup>−/−</jats:sup> mice. Na<jats:sub>v</jats:sub>1.8 inhibitor A‐803467, but not <jats:styled-content style="fixed-case">TTX</jats:styled-content>, diminished the hyperexcitability and blocked repetitive <jats:styled-content style="fixed-case">AP</jats:styled-content> firing of these neurons.</jats:p></jats:sec><jats:sec><jats:title>Conclusion</jats:title><jats:p>Our results indicate that histamine participates in acute pain modulation in a dose‐related manner. The regulation of Na<jats:sub>v</jats:sub>1.8 expression and the excitability of nociceptive primary afferent neurons may be involved in the underlying mechanisms.</jats:p></jats:sec> |
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| spelling | Yu, Jie Fang, Qi Lou, Guo‐Dong Shou, Wen‐Ting Yue, Jia‐Xing Tang, Ying‐Ying Hou, Wei‐Wei Xu, Tian‐Le Ohtsu, Hiroshi Zhang, Shi‐Hong Chen, Zhong 1755-5930 1755-5949 Wiley Pharmacology (medical) Physiology (medical) Psychiatry and Mental health Pharmacology http://dx.doi.org/10.1111/cns.12134 <jats:title>Summary</jats:title><jats:sec><jats:title>Aims</jats:title><jats:p>To explore the role of histamine in acute pain perception and its possible mechanisms.</jats:p></jats:sec><jats:sec><jats:title>Methods</jats:title><jats:p>Pain‐like behaviors induced by four types of noxious stimuli (hot‐plate, tail‐pressure, acetic acid, and formalin) were accessed in mice. Na<jats:sub>v</jats:sub>1.8 expression and functions in primary afferent neurons were compared between histidine decarboxylase knockout (<jats:styled-content style="fixed-case">HDC</jats:styled-content><jats:sup>−/−</jats:sup>) mice and their wild‐types.</jats:p></jats:sec><jats:sec><jats:title>Results</jats:title><jats:p><jats:styled-content style="fixed-case">HDC</jats:styled-content><jats:sup>−/−</jats:sup> mice, lacking in endogenous histamine, showed elevated sensitivity to all these noxious stimuli, as compared with the wild‐types. In addition, a depletion of endogenous histamine with α‐fluoromethylhistidine (α‐<jats:styled-content style="fixed-case">FMH</jats:styled-content>), a specific <jats:styled-content style="fixed-case">HDC</jats:styled-content> inhibitor, or feeding mice a low‐histamine diet also enhanced nociception in the wild‐types. Na<jats:sub>v</jats:sub>1.8 expression in primary afferent neurons was increased both in <jats:styled-content style="fixed-case">HDC</jats:styled-content><jats:sup>−/−</jats:sup> and in α‐<jats:styled-content style="fixed-case">FMH</jats:styled-content>‐treated wild‐type mice. A higher Na<jats:sub>v</jats:sub>1.8 current density, a lower action potential (<jats:styled-content style="fixed-case">AP</jats:styled-content>) threshold, and a higher firing rate in response to suprathreshold stimulation were observed in nociception‐related small <jats:styled-content style="fixed-case">DRG</jats:styled-content> neurons of <jats:styled-content style="fixed-case">HDC</jats:styled-content><jats:sup>−/−</jats:sup> mice. Na<jats:sub>v</jats:sub>1.8 inhibitor A‐803467, but not <jats:styled-content style="fixed-case">TTX</jats:styled-content>, diminished the hyperexcitability and blocked repetitive <jats:styled-content style="fixed-case">AP</jats:styled-content> firing of these neurons.</jats:p></jats:sec><jats:sec><jats:title>Conclusion</jats:title><jats:p>Our results indicate that histamine participates in acute pain modulation in a dose‐related manner. The regulation of Na<jats:sub>v</jats:sub>1.8 expression and the excitability of nociceptive primary afferent neurons may be involved in the underlying mechanisms.</jats:p></jats:sec> Histamine Modulation of Acute Nociception Involves Regulation of Na<sub>v</sub>1.8 in Primary Afferent Neurons in Mice CNS Neuroscience & Therapeutics |
| spellingShingle | Yu, Jie, Fang, Qi, Lou, Guo‐Dong, Shou, Wen‐Ting, Yue, Jia‐Xing, Tang, Ying‐Ying, Hou, Wei‐Wei, Xu, Tian‐Le, Ohtsu, Hiroshi, Zhang, Shi‐Hong, Chen, Zhong, CNS Neuroscience & Therapeutics, Histamine Modulation of Acute Nociception Involves Regulation of Nav1.8 in Primary Afferent Neurons in Mice, Pharmacology (medical), Physiology (medical), Psychiatry and Mental health, Pharmacology |
| title | Histamine Modulation of Acute Nociception Involves Regulation of Nav1.8 in Primary Afferent Neurons in Mice |
| title_full | Histamine Modulation of Acute Nociception Involves Regulation of Nav1.8 in Primary Afferent Neurons in Mice |
| title_fullStr | Histamine Modulation of Acute Nociception Involves Regulation of Nav1.8 in Primary Afferent Neurons in Mice |
| title_full_unstemmed | Histamine Modulation of Acute Nociception Involves Regulation of Nav1.8 in Primary Afferent Neurons in Mice |
| title_short | Histamine Modulation of Acute Nociception Involves Regulation of Nav1.8 in Primary Afferent Neurons in Mice |
| title_sort | histamine modulation of acute nociception involves regulation of na<sub>v</sub>1.8 in primary afferent neurons in mice |
| title_unstemmed | Histamine Modulation of Acute Nociception Involves Regulation of Nav1.8 in Primary Afferent Neurons in Mice |
| topic | Pharmacology (medical), Physiology (medical), Psychiatry and Mental health, Pharmacology |
| url | http://dx.doi.org/10.1111/cns.12134 |