Search tips
Search criteria

Results 1-3 (3)

Clipboard (0)

Select a Filter Below

more »
Year of Publication
Document Types
1.  Electro-acupuncture on functional peripheral nerve regeneration in mice: a behavioural study 
The improvement of axonal regeneration is a major objective in the treatment of peripheral nerve injuries. The aim of this study was to evaluate the effects of electro-acupuncture on the functional recovery of sensorimotor responses following left sciatic nerve crush in mice.
Sciatic nerve crush was performed on seven week old female mice. Following the injury, the control group was untreated while the experimental group received an electro-acupuncture application to the injured limb under isoflurane anesthesia at acupoints GB 30 and GB 34. Mechanical and heat sensitivity tests were performed to evaluate sensory recovery. Gait analysis was performed to assess sensorimotor recovery.
Our results show that normal sensory recovery is achieved within five to six weeks with a two-week period of pain preceding the recovery to normal sensitivity levels. While electro-acupuncture did not accelerate sensory recovery, it did alleviate pain-related behaviour but only when applied during this period. Application before the development of painful symptoms did not prevent their occurrence. The analysis of gait in relation to the sensory tests suggests that the electro-acupuncture specifically improved motor recovery.
This study demonstrates that electro-acupuncture exerts a positive influence on motor recovery and is efficient in the treatment of pain symptoms that develop during target re-innervation.
PMCID: PMC3479081  PMID: 22937957
Sciatic nerve; Crush; Nerve injury; Pain; Sensorimotor
2.  Regulation of the Na,K-ATPase Gamma-Subunit FXYD2 by Runx1 and Ret Signaling in Normal and Injured Non-Peptidergic Nociceptive Sensory Neurons 
PLoS ONE  2012;7(1):e29852.
Dorsal root ganglia (DRGs) contain the cell bodies of sensory neurons which relay nociceptive, thermoceptive, mechanoceptive and proprioceptive information from peripheral tissues toward the central nervous system. These neurons establish constant communication with their targets which insures correct maturation and functioning of the somato-sensory nervous system. Interfering with this two-way communication leads to cellular, electrophysiological and molecular modifications that can eventually cause neuropathic conditions. In this study we reveal that FXYD2, which encodes the gamma-subunit of the Na,K-ATPase reported so far to be mainly expressed in the kidney, is induced in the mouse DRGs at postnatal stages where it is restricted specifically to the TrkB-expressing mechanoceptive and Ret-positive/IB4-binding non-peptidergic nociceptive neurons. In non-peptidergic nociceptors, we show that the transcription factor Runx1 controls FXYD2 expression during the maturation of the somato-sensory system, partly through regulation of the tyrosine kinase receptor Ret. Moreover, Ret signaling maintains FXYD2 expression in adults as demonstrated by the axotomy-induced down-regulation of the gene that can be reverted by in vivo delivery of GDNF family ligands. Altogether, these results establish FXYD2 as a specific marker of defined sensory neuron subtypes and a new target of the Ret signaling pathway during normal maturation of the non-peptidergic nociceptive neurons and after sciatic nerve injury.
PMCID: PMC3258241  PMID: 22253804
3.  Best1 is a gene regulated by nerve injury and required for Ca2+-activated Cl− current expression in axotomized sensory neurons 
We investigated the molecular determinants of Ca2+-activated chloride current (CaCC) expressed in adult sensory neurons following a nerve injury. Dorsal root ganglia express the transcripts of three gene families known to induce CaCCs in heterologous systems: bestrophin, tweety and TMEM16. We found with quantitative transcriptional analysis and in situ hybridization that nerve injury induced upregulation of solely bestrophin-1 transcripts in sensory neurons. Gene screening with RNA interference in single neurons demonstrated that mouse Best1 is required for the expression of CaCC in injured sensory neurons. Transfecting injured sensory neurons with bestrophin-1 mutants inhibited endogenous CaCC. Exogenous expression of the fusion protein GFP-Bestrophin-1 in naive neurons demonstrated a plasma membrane localization of the protein that generates a CaCC with biophysical and pharmacological properties similar to endogenous CaCC. Our data suggest that Best1 belongs to a group of genes upregulated by nerve injury and supports functional CaCC expression in injured sensory neurons.
PMCID: PMC2761749  PMID: 19675239
Bestrophin; chloride current; chloride homeostasis; injury; regeneration; DRG

Results 1-3 (3)