Nerve injury induced activation of fast-conducting high threshold mechanoreceptors predicts non-reflexive pain related behavior

[Display omitted] •Graded fast conducting high threshold mechanoreceptor activation can be elicited.•Induced neuronal activity in this subset is further increased after nerve injury.•Activity of these neurons predicts pain related place aversion.•This nerve subset may contribute to pain beyond acute...

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Bibliographic Details
Published inNeuroscience letters Vol. 632; pp. 44 - 49
Main Authors Boada, M. Danilo, Martin, Thomas J., Ririe, Douglas G.
Format Journal Article
LanguageEnglish
Published Ireland Elsevier B.V 06.10.2016
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Summary:[Display omitted] •Graded fast conducting high threshold mechanoreceptor activation can be elicited.•Induced neuronal activity in this subset is further increased after nerve injury.•Activity of these neurons predicts pain related place aversion.•This nerve subset may contribute to pain beyond acute pain signaling.•Consideration of these neurons in chronic pain may further knowledge and treatment. The role of specific subsets of peripheral nerves in pain related behavior remains unclear. To better understand the contribution of differential activation of fast-conducting, high-threshold mechanoreceptor (AHTMR) input, we hypothesized that neuronal activation would be distinct with nerve injury, and that nociceptive input would predictt behavior in the freely exploring animal. A series of surfaces was used to deliver mechanical input to the hindpaws of rats upon voluntary movement and exploration. Neuronal activation increased as apex surface decreased (0.2, 0.6, 1.0 and 1.5mm) using in vivo recording in L4 DRG neurons, and this relationship was enhanced following partial ligation of L5 (pSNL). In behaving animals, apex size was correlated to time spent on each surface following pSNL, but not with sham. Morphine normalized the discriminatory behavior following pSNL. These data indicate that noxious mechanical activation of AHTMR upon normal movement predicts behavior using paradigms that do not rely on reflexive withdrawal responses suggesting that AHTMR activation and central nervous system input contribute to higher order pain behavior after nerve injury beyond the immediate early pain input long attributed to these neurons.
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ISSN:0304-3940
1872-7972
DOI:10.1016/j.neulet.2016.08.029