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

2016 ◽  
Vol 43 (6) ◽  
pp. 802-810 ◽  
Author(s):  
Nathalie Pham-Dang ◽  
Amélie Descheemaeker ◽  
Radhouane Dallel ◽  
Alain Artola
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Dorsal Horn ◽  
Mechanical Allodynia ◽  
Kinase C ◽  
Medullary Dorsal Horn

Protein kinase C gamma-like immunoreactivity of trigeminothalamic neurons in the medullary dorsal horn of the rat

2001 ◽  
Vol 913 (2) ◽  
pp. 159-164 ◽  
Author(s):  
Yun-Qing Li ◽  
Jin-Lian Li ◽  
Hui Li ◽  
Takeshi Kaneko ◽  
Noboru Mizuno
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Dorsal Horn ◽  
Kinase C ◽  
Medullary Dorsal Horn ◽  
Protein Kinase C Gamma

Protein kinase C gamma-like immunoreactivity in the substantia gelatinosa of the medullary dorsal horn of the rat

2001 ◽  
Vol 311 (3) ◽  
pp. 185-188 ◽  
Author(s):  
Jin-Lian Li ◽  
Yun-Qing Li ◽  
Sakashi Nomura ◽  
Takeshi Kaneko ◽  
Noboru Mizuno
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Dorsal Horn ◽  
Substantia Gelatinosa ◽  
Kinase C ◽  
Medullary Dorsal Horn ◽  
Protein Kinase C Gamma

Protein Kinase C γ Interneurons Mediate C-fiber–induced Orofacial Secondary Static Mechanical Allodynia, but Not C-fiber–induced Nociceptive Behavior

2016 ◽  
Vol 124 (5) ◽  
pp. 1136-1152 ◽  
Author(s):  
Cedric Peirs ◽  
Nathalie Bourgois ◽  
Alain Artola ◽  
Radhouane Dallel
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Mechanical Allodynia ◽  
Molecular Mechanisms ◽  
Spontaneous Pain ◽  
Secondary Hyperalgesia ◽  
Neuronal Activation ◽  
Kinase C ◽  
C Fiber ◽  
Static Mechanical

Abstract Background Tissue injury enhances pain sensitivity both at the site of tissue damage and in surrounding uninjured skin (secondary hyperalgesia). Secondary hyperalgesia encompasses several pain symptoms including pain to innocuous punctate stimuli or static mechanical allodynia. How injury-induced barrage from C-fiber nociceptors produces secondary static mechanical allodynia has not been elucidated. Methods Combining behavioral, immunohistochemical, and Western blot analysis, the authors investigated the cell and molecular mechanisms underlying the secondary static mechanical allodynia in the rat medullary dorsal horn (MDH) using the capsaicin model (n = 4 to 5 per group). Results Intradermal injection of capsaicin (25 μg) into the vibrissa pad produces a spontaneous pain and a secondary static mechanical allodynia. This allodynia is associated with the activation of a neuronal network encompassing lamina I–outer lamina III, including interneurons expressing the γ isoform of protein kinase C (PKCγ) within inner lamina II (IIi) of MDH. PKCγ is concomitantly phosphorylated (+351.4 ± 79.2%, mean ± SD; P = 0.0003). Mechanical allodynia and innocuous punctate stimulus–evoked laminae I to III neuronal activation can be replicated after intracisternally applied γ-aminobutyric acid receptor type A (GABAA) antagonist (bicuculline: 0.05 μg) or reactive oxygen species (ROS) donor (tert-butyl hydroperoxide: 50 to 250 ng). Conversely, intracisternal PKCγ antagonist, GABAA receptor agonist, or ROS scavenger prevent capsaicin-induced static mechanical allodynia and neuronal activation. Conclusions Sensitization of lamina IIi PKCγ interneurons is required for the manifestation of secondary static mechanical allodynia but not for spontaneous pain. Such sensitization is driven by ROS and GABAAergic disinhibition. ROS released during intense C-fiber nociceptor activation might produce a GABAAergic disinhibition of PKCγ interneurons. Innocuous punctate inputs carried by Aδ low-threshold mechanoreceptors onto PKCγ interneurons can then gain access to the pain transmission circuitry of superficial MDH, producing pain.

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