Evidence map›Paper›PMID 29392218›Full record

ArticlePain reports2017

Rat model of cancer-induced bone pain: changes in nonnociceptive sensory neurons in vivo.

Yong Fang Zhu, Robert Ungard, Natalie Zacal, Jan D Huizinga, James L Henry, Gurmit Singh

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PubMed Full text at PMC Publisher
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Article in Pain reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

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0cells of the map it votes in
13citing papers in PubMed
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1 · What the graph read from it

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2 · The registry

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3 · Its place in the literature

Who cites it

13 citing papers in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

6 authors.

Yong Fang ZhuMichael G. DeGroote Institute for Pain Research and Care, McMaster University, Hamilton, ON, Canada.
Robert UngardMichael G. DeGroote Institute for Pain Research and Care, McMaster University, Hamilton, ON, Canada.
Natalie ZacalMichael G. DeGroote Institute for Pain Research and Care, McMaster University, Hamilton, ON, Canada.
Jan D HuizingaDepartment of Medicine, Farncombe Family Digestive Health Research Institute, McMaster University, Hamilton, ON, Canada.
James L HenryDepartment of Psychiatry and Behavioural Neurosciences, McMaster University, Hamilton, ON, Canada.
Gurmit SinghMichael G. DeGroote Institute for Pain Research and Care, McMaster University, Hamilton, ON, Canada.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionClinical data on cancer-induced bone pain (CIBP) suggest extensive changes in sensory function. In a previous investigation of an animal model of CIBP, we have observed that changes in intrinsic membrane properties and excitability of dorsal root ganglion (DRG) nociceptive neurons correspond to mechanical allodynia and hyperalgesia.

objectivesTo investigate the mechanisms underlying changes in nonnociceptive sensory neurons in this model, we have compared the electrophysiological properties of primary nonnociceptive sensory neurons at <1 and >2 weeks after CIBP model induction with properties in sham control animals.

methodsCopenhagen rats were injected with 10

resultsThe mechanical withdrawal threshold progressively decreased in CIBP model rats. At <1 week after model induction, there were no changes observed in nonnociceptive Aβ-fiber DRG neurons between CIBP model rats and sham rats. However, at >2 weeks, the Aβ-fiber low-threshold mechanoreceptors (LTMs) in CIBP model rats exhibited a slowing of the dynamics of action potential (AP) genesis, including wider AP duration and lower AP amplitude compared with sham rats. Furthermore, enhanced excitability of Aβ-fiber LTM neurons was observed as an excitatory discharge in response to intracellular injection of depolarizing current into the soma.

conclusionAfter induction of the CIBP model, Aβ-fiber LTMs at >2 weeks but not <1 week had undergone changes in electrophysiological properties. Importantly, changes observed are consistent with observations in models of peripheral neuropathy. Thus, Aβ-fiber nonnociceptive primary sensory neurons might be involved in the peripheral sensitization and tumor-induced tactile hypersensitivity in CIBP.

Indexed as

Cancer-induced bone painElectrophysiologyRat modelSensory neurons

Identifiers

PMID29392218
PMCPMC5741358

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.