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Ligation of mouse L4 and L5 spinal nerves produces robust allodynia without major motor function deficit.
Behav Brain Res. 2015 Jan 01; 276:99-110.BB

Abstract

Spinal nerve L5/L6 ligation (SNL) in rats has become the standard for mechanistic studies of peripheral neuropathy and screening for novel analgesics. Conventional SNL in our hybrid mice resulted in a wide range of allodynia. Anatomical evaluation indicated that a variable number of lumbar vertebrae existed, resulting in L4/L5 or L5/L6 being ligated. Surprisingly, L4/L5 ligation did not result in ipsilateral hind limb paralysis and produced robust allodynia. Following a recent report that the mouse L4 neural segment is homologous with rat L5 we generated L4, L5 or both L4 and L5 (L4/L5) ligations in C57 mice after establishing a modified set of surgical landmarks. In contrast to rats, L4 ligation in these mice did not result in hind limb paralysis. Robust allodynia was observed in all three ligation groups. Nerve degeneration confirmed that L4 and L5, respectively, are primary contributors to the tibial and sural branches of the sciatic nerve in mice. A larger von Frey sensitive area reflected the wider distribution of Wallerian degeneration in the hindlimb of L4- compared to L5-ligated mice. Ligation of mouse L4 and L5 spinal nerves produces consistent, robust neuropathic pain behaviors and is suitable as a model for investigating mechanisms of neuropathic pain and for testing of novel analgesics. Gabapentin, used as a validation drug in neuropathic pain models and as a reference compound for novel analgesics, significantly reduced allodynia in the mice tested (L4/L5 ligations). Given the ease of surgery, robust allodynia, and larger von Frey sensitive area, we conclude that combined ligation of spinal nerves L4 and L5 optimizes the SNL model in mice.

Authors+Show Affiliations

Neuroscience Research, Lexicon Pharmaceuticals Inc., The Woodlands, TX 77381, USA.Neuroscience Research, Lexicon Pharmaceuticals Inc., The Woodlands, TX 77381, USA.Neuroscience Research, Lexicon Pharmaceuticals Inc., The Woodlands, TX 77381, USA.Neuroscience Research, Lexicon Pharmaceuticals Inc., The Woodlands, TX 77381, USA.Neuroscience Research, Lexicon Pharmaceuticals Inc., The Woodlands, TX 77381, USA.Neuroscience Research, Lexicon Pharmaceuticals Inc., The Woodlands, TX 77381, USA.Neuroscience Research, Lexicon Pharmaceuticals Inc., The Woodlands, TX 77381, USA. Electronic address: indrani.rajan@lonestar.edu.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

24786331

Citation

Ye, Gui-Lan, et al. "Ligation of Mouse L4 and L5 Spinal Nerves Produces Robust Allodynia Without Major Motor Function Deficit." Behavioural Brain Research, vol. 276, 2015, pp. 99-110.
Ye GL, Savelieva KV, Vogel P, et al. Ligation of mouse L4 and L5 spinal nerves produces robust allodynia without major motor function deficit. Behav Brain Res. 2015;276:99-110.
Ye, G. L., Savelieva, K. V., Vogel, P., Baker, K. B., Mason, S., Lanthorn, T. H., & Rajan, I. (2015). Ligation of mouse L4 and L5 spinal nerves produces robust allodynia without major motor function deficit. Behavioural Brain Research, 276, 99-110. https://doi.org/10.1016/j.bbr.2014.04.039
Ye GL, et al. Ligation of Mouse L4 and L5 Spinal Nerves Produces Robust Allodynia Without Major Motor Function Deficit. Behav Brain Res. 2015 Jan 1;276:99-110. PubMed PMID: 24786331.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Ligation of mouse L4 and L5 spinal nerves produces robust allodynia without major motor function deficit. AU - Ye,Gui-Lan, AU - Savelieva,Katerina V, AU - Vogel,Peter, AU - Baker,Kevin B, AU - Mason,Sara, AU - Lanthorn,Thomas H, AU - Rajan,Indrani, Y1 - 2014/04/29/ PY - 2014/01/28/received PY - 2014/04/16/revised PY - 2014/04/21/accepted PY - 2014/5/3/entrez PY - 2014/5/3/pubmed PY - 2015/8/12/medline KW - Mouse neuropathic pain KW - Neurogenic atrophy KW - Spinal nerve ligation KW - Tactile allodynia KW - Wallerian degeneration KW - von Frey SP - 99 EP - 110 JF - Behavioural brain research JO - Behav Brain Res VL - 276 N2 - Spinal nerve L5/L6 ligation (SNL) in rats has become the standard for mechanistic studies of peripheral neuropathy and screening for novel analgesics. Conventional SNL in our hybrid mice resulted in a wide range of allodynia. Anatomical evaluation indicated that a variable number of lumbar vertebrae existed, resulting in L4/L5 or L5/L6 being ligated. Surprisingly, L4/L5 ligation did not result in ipsilateral hind limb paralysis and produced robust allodynia. Following a recent report that the mouse L4 neural segment is homologous with rat L5 we generated L4, L5 or both L4 and L5 (L4/L5) ligations in C57 mice after establishing a modified set of surgical landmarks. In contrast to rats, L4 ligation in these mice did not result in hind limb paralysis. Robust allodynia was observed in all three ligation groups. Nerve degeneration confirmed that L4 and L5, respectively, are primary contributors to the tibial and sural branches of the sciatic nerve in mice. A larger von Frey sensitive area reflected the wider distribution of Wallerian degeneration in the hindlimb of L4- compared to L5-ligated mice. Ligation of mouse L4 and L5 spinal nerves produces consistent, robust neuropathic pain behaviors and is suitable as a model for investigating mechanisms of neuropathic pain and for testing of novel analgesics. Gabapentin, used as a validation drug in neuropathic pain models and as a reference compound for novel analgesics, significantly reduced allodynia in the mice tested (L4/L5 ligations). Given the ease of surgery, robust allodynia, and larger von Frey sensitive area, we conclude that combined ligation of spinal nerves L4 and L5 optimizes the SNL model in mice. SN - 1872-7549 UR - https://www.unboundmedicine.com/medline/citation/24786331/Ligation_of_mouse_L4_and_L5_spinal_nerves_produces_robust_allodynia_without_major_motor_function_deficit_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0166-4328(14)00257-5 DB - PRIME DP - Unbound Medicine ER -