Activation of medullary dorsal horn γ isoform of protein kinase C interneurons is essential to the development of both static and dynamic facial mechanical allodynia.
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| Title: | Activation of medullary dorsal horn γ isoform of protein kinase C interneurons is essential to the development of both static and dynamic facial mechanical allodynia. |
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| Authors: | Pham‐Dang, Nathalie, Descheemaeker, Amélie, Dallel, Radhouane, Artola, Alain, Barrot, Michel |
| Source: | European Journal of Neuroscience. Mar2016, Vol. 43 Issue 6, p802-810. 9p. 1 Color Photograph, 1 Chart, 3 Graphs. |
| Subjects: | Protein kinase C, Interneurons, Allodynia, Phorbol esters, Neural transmission, Therapeutics |
| Abstract: | The γ isoform of protein kinase C ( PKCγ), which is concentrated in a specific class of interneurons within inner lamina II ( IIi) of the spinal dorsal horn and medullary dorsal horn ( MDH), is known to be involved in the development of mechanical allodynia, a widespread and intractable symptom of inflammatory or neuropathic pain. However, although genetic and pharmacological impairment of PKCγ were shown to prevent mechanical allodynia in animal models of pain, after nerve injury or reduced inhibition, the functional consequences of PKCγ activation alone on mechanical sensitivity are still unknown. Using behavioural and anatomical approaches in the rat MDH, we tested whether PKCγ activation in naive animals is sufficient for the establishment of mechanical allodynia. Intracisternal injection of the phorbol ester, 12,13-dibutyrate concomitantly induced static as well as dynamic facial mechanical allodynia. Monitoring neuronal activity within the MDH with phospho-extracellular signal-regulated kinases 1 and 2 immunoreactivity revealed that activation of both lamina I-outer lamina II and IIi-outer lamina III neurons, including lamina IIi PKCγ-expressing interneurons, was associated with the manifestation of mechanical allodynia. Phorbol ester, 12,13-dibutyrate-induced mechanical allodynia and associated neuronal activations were all prevented by inhibiting selectively segmental PKCγ with KIG31-1. Our findings suggest that PKCγ activation, without any other experimental manipulation, is sufficient for the development of static and dynamic mechanical allodynia. Lamina IIi PKCγ interneurons have been shown to be directly activated by low-threshold mechanical inputs carried by myelinated afferents. Thus, the level of PKCγ activation within PKCγ interneurons might gate the transmission of innocuous mechanical inputs to lamina I, nociceptive output neurons, thus turning touch into pain. [ABSTRACT FROM AUTHOR] |
| Copyright of European Journal of Neuroscience is the property of Wiley-Blackwell 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.) | |
| Database: | Psychology and Behavioral Sciences Collection |
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| Header | DbId: pbh DbLabel: Psychology and Behavioral Sciences Collection An: 113900700 AccessLevel: 6 PubType: Academic Journal PubTypeId: academicJournal PreciseRelevancyScore: 0 |
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| Items | – Name: Title Label: Title Group: Ti Data: Activation of medullary dorsal horn γ isoform of protein kinase C interneurons is essential to the development of both static and dynamic facial mechanical allodynia. – Name: Author Label: Authors Group: Au Data: <searchLink fieldCode="AR" term="%22Pham‐Dang%2C+Nathalie%22">Pham‐Dang, Nathalie</searchLink><br /><searchLink fieldCode="AR" term="%22Descheemaeker%2C+Amélie%22">Descheemaeker, Amélie</searchLink><br /><searchLink fieldCode="AR" term="%22Dallel%2C+Radhouane%22">Dallel, Radhouane</searchLink><br /><searchLink fieldCode="AR" term="%22Artola%2C+Alain%22">Artola, Alain</searchLink><br /><searchLink fieldCode="AR" term="%22Barrot%2C+Michel%22">Barrot, Michel</searchLink> – Name: TitleSource Label: Source Group: Src Data: <searchLink fieldCode="JN" term="%22European+Journal+of+Neuroscience%22">European Journal of Neuroscience</searchLink>. Mar2016, Vol. 43 Issue 6, p802-810. 9p. 1 Color Photograph, 1 Chart, 3 Graphs. – Name: Subject Label: Subjects Group: Su Data: <searchLink fieldCode="DE" term="%22Protein+kinase+C%22">Protein kinase C</searchLink><br /><searchLink fieldCode="DE" term="%22Interneurons%22">Interneurons</searchLink><br /><searchLink fieldCode="DE" term="%22Allodynia%22">Allodynia</searchLink><br /><searchLink fieldCode="DE" term="%22Phorbol+esters%22">Phorbol esters</searchLink><br /><searchLink fieldCode="DE" term="%22Neural+transmission%22">Neural transmission</searchLink><br /><searchLink fieldCode="DE" term="%22Therapeutics%22">Therapeutics</searchLink> – Name: Abstract Label: Abstract Group: Ab Data: The γ isoform of protein kinase C ( PKCγ), which is concentrated in a specific class of interneurons within inner lamina II ( IIi) of the spinal dorsal horn and medullary dorsal horn ( MDH), is known to be involved in the development of mechanical allodynia, a widespread and intractable symptom of inflammatory or neuropathic pain. However, although genetic and pharmacological impairment of PKCγ were shown to prevent mechanical allodynia in animal models of pain, after nerve injury or reduced inhibition, the functional consequences of PKCγ activation alone on mechanical sensitivity are still unknown. Using behavioural and anatomical approaches in the rat MDH, we tested whether PKCγ activation in naive animals is sufficient for the establishment of mechanical allodynia. Intracisternal injection of the phorbol ester, 12,13-dibutyrate concomitantly induced static as well as dynamic facial mechanical allodynia. Monitoring neuronal activity within the MDH with phospho-extracellular signal-regulated kinases 1 and 2 immunoreactivity revealed that activation of both lamina I-outer lamina II and IIi-outer lamina III neurons, including lamina IIi PKCγ-expressing interneurons, was associated with the manifestation of mechanical allodynia. Phorbol ester, 12,13-dibutyrate-induced mechanical allodynia and associated neuronal activations were all prevented by inhibiting selectively segmental PKCγ with KIG31-1. Our findings suggest that PKCγ activation, without any other experimental manipulation, is sufficient for the development of static and dynamic mechanical allodynia. Lamina IIi PKCγ interneurons have been shown to be directly activated by low-threshold mechanical inputs carried by myelinated afferents. Thus, the level of PKCγ activation within PKCγ interneurons might gate the transmission of innocuous mechanical inputs to lamina I, nociceptive output neurons, thus turning touch into pain. [ABSTRACT FROM AUTHOR] – Name: AbstractSuppliedCopyright Label: Group: Ab Data: <i>Copyright of European Journal of Neuroscience is the property of Wiley-Blackwell 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: BibEntity: Identifiers: – Type: doi Value: 10.1111/ejn.13165 Languages: – Code: eng Text: English PhysicalDescription: Pagination: PageCount: 9 StartPage: 802 Subjects: – SubjectFull: Protein kinase C Type: general – SubjectFull: Interneurons Type: general – SubjectFull: Allodynia Type: general – SubjectFull: Phorbol esters Type: general – SubjectFull: Neural transmission Type: general – SubjectFull: Therapeutics Type: general Titles: – TitleFull: Activation of medullary dorsal horn γ isoform of protein kinase C interneurons is essential to the development of both static and dynamic facial mechanical allodynia. Type: main BibRelationships: HasContributorRelationships: – PersonEntity: Name: NameFull: Pham‐Dang, Nathalie – PersonEntity: Name: NameFull: Descheemaeker, Amélie – PersonEntity: Name: NameFull: Dallel, Radhouane – PersonEntity: Name: NameFull: Artola, Alain – PersonEntity: Name: NameFull: Barrot, Michel IsPartOfRelationships: – BibEntity: Dates: – D: 15 M: 03 Text: Mar2016 Type: published Y: 2016 Identifiers: – Type: issn-print Value: 0953816X Numbering: – Type: volume Value: 43 – Type: issue Value: 6 Titles: – TitleFull: European Journal of Neuroscience Type: main |
| ResultId | 1 |
