Chronic constriction injury of the infraorbital nerve in the rat using modified syringe needle

Kernisant, Melanie; Gear, Robert W.; Jasmin, Luc; Vit, Jean-Philippe; Ohara, Peter T.

doi:10.1016/j.jneumeth.2008.04.013

Cited by 60 publications

(55 citation statements)

References 19 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…3B. Importantly, it is also of note that our results show a role of NMDA, but not AMPA, receptors in the DRG in the development of inflammatory hyperalgesia, whereas those authors have shown the involvement of other types of GLU receptors in a model of neuropathic pain [i.e., chronic constriction injury (40,41)]. These findings suggest the involvement of different types of GLU receptors in the DRG during inflammatory and neuropathic hyperalgesia.…”

Section: Resultscontrasting

confidence: 38%

Inflammatory sensitization of nociceptors depends on activation of NMDA receptors in DRG satellite cells

Ferrari

Lotufo

Araldi

et al. 2014

Proc. Natl. Acad. Sci. U.S.A.

View full text Add to dashboard Cite

The present study evaluated the role of N-methyl-D-aspartate receptors (NMDARs) expressed in the dorsal root ganglia (DRG) in the inflammatory sensitization of peripheral nociceptor terminals to mechanical stimulation. Injection of NMDA into the fifth lumbar (L5)-DRG induced hyperalgesia in the rat hind paw with a profile similar to that of intraplantar injection of prostaglandin E 2 (PGE 2 ), which was significantly attenuated by injection of the NMDAR antagonist D(-)-2-amino-5-phosphonopentanoic acid (D-AP-5) in the L5-DRG. Moreover, blockade of DRG AMPA receptors by the antagonist 6,7-dinitroquinoxaline-2,3-dione had no effect in the PGE 2 -induced hyperalgesia in thepaw, showing specific involvement of NMDARs in this modulatory effect and suggesting that activation of NMDAR in the DRG plays an important role in the peripheral inflammatory hyperalgesia. In following experiments we observed attenuation of PGE 2 -induced hyperalgesia in the paw by the knockdown of NMDAR subunits NR1, NR2B, NR2D, and NR3A with antisense-oligodeoxynucleotide treatment in the DRG. Also, in vitro experiments showed that the NMDAinduced sensitization of cultured DRG neurons depends on satellite cell activation and on those same NMDAR subunits, suggesting their importance for the PGE 2 -induced hyperalgesia. In addition, fluorescent calcium imaging experiments in cultures of DRG cells showed induction of calcium transients by glutamate or NMDA only in satellite cells, but not in neurons. Together, the present results suggest that the mechanical inflammatory nociceptor sensitization is dependent on glutamate release at the DRG and subsequent NMDAR activation in satellite glial cells, supporting the idea that the peripheral hyperalgesia is an event modulated by a glutamatergic system in the DRG.T he involvement of excitatory amino acids in the transmission of the nociceptive information from the primary afferent neurons to the spinal cord is, at present, supported by an immense number of studies (1-3). In fact, a role of the amino acid glutamate (GLU) as a synaptic mediator has been demonstrated by electrophysiological experiments that showed its release by stimulation and consequent increase in the probability that the target cell will fire an action potential (3, 4). In addition, glutamatergic receptors, especially the N-methyl-D-aspartate receptor (NMDAR), detected throughout the entire nervous system (5, 6), have been associated with the development and maintenance of spinal cord neuron sensitization (7,8). Stimulation of spinal neurons by GLU through NMDARs was also associated to inflammatory processes (3, 9). For instance, sensitization of spinal nerves has been frequently related to the wind-up phenomenon, an increase in the electrical activity of spinal cord neurons and pain sensation independent of primary nociceptor input (10).The detection of glutamatergic receptors in the presynaptic membrane of afferent fibers associated with nociception and hyperalgesia raised the hypothesis that GLU released into the synaptic cleft cou...

show abstract

Section: Resultscontrasting

confidence: 38%

Inflammatory sensitization of nociceptors depends on activation of NMDA receptors in DRG satellite cells

Ferrari

Lotufo

Araldi

et al. 2014

Proc. Natl. Acad. Sci. U.S.A.

View full text Add to dashboard Cite

show abstract

“…IoN-CCI 25 , the application of complete Freund’s adjuvant (CFA) to the orbital portion of the IoN 3 , and unilateral partial ligation of the IoN (pIONL) 1, 28 are three commonly used animal models to study trigeminal neuropathic pain. All IoN-CCI procedures described and used by others are also complex and difficult to perform 10, 12, 13, 25 . In this report, we showed an improved model of IoN-CCI by 1) using a 0.5 cm facial incision to access the IoN trunk outside the orbital cavity and 2) placing two ligatures at the distal IoN just before the IoN branches into the whisker pad.…”

Section: Discussionmentioning

confidence: 99%

“…Current literature indicates that chronic constriction injury of the IoN has been performed by placing two chromic gut ligatures on the IoN trunk either inside 13, 25 or outside 10, 12 the orbital cavity. Both midline 25 and eye lid 13 incisions have been used to gain access to the IoN segment inside the orbital cavity, and in either case the orbital contents are affected. The placement of ligatures on the intraorbital segment of the IoN presses the orbital contents and may cause eye discomfort, leading to increased grooming activities.…”

Section: Discussionmentioning

confidence: 99%

“…In contrast, the nociceptive behavior of rats subjected to previous IoN-CCI procedures varies depending on the specific type of procedure used in different studies 6, 13, 16, 17 . Some studies showed that IoN-CCI rats exhibited an early phase hyposensitivity and a late phase hypersensitivity to mechanical stimulation in the IoN territory 13, 25 . The early phase hyposensitivity lasted from 3 days 13 to 14 days 25 .…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

An Improved Rodent Model of Trigeminal Neuropathic Pain by Unilateral Chronic Constriction Injury of Distal Infraorbital Nerve

Ding

You

Shen

et al. 2017

The Journal of Pain

View full text Add to dashboard Cite

The number of studies on trigeminal nerve injury using animal models remains limited. A rodent model of trigeminal neuropathic pain was first developed in the 1994, in which chronic constriction injury is induced by ligation of the infraorbital nerve (IoN-CCI). This animal model has served as a major tool to study trigeminal neuropathic pain. Unfortunately, the surgical procedure in this model is complicated and far more difficult than ligation of peripheral nerves (e.g. sciatic nerve). The aim of this study was to improve on the current surgical procedure of IoN ligation to induce trigeminal neuropathic pain in rats. We demonstrate that the IoN can be readily accessed through a small facial incision. Chronic constriction injury can be induced by ligation of a segment at the distal infraorbital nerve (dIoN-CCI). This dIoN-CCI procedure is simple, minimally invasive and time-saving. Our data show that the dIoN-CCI procedure consistently induced both acute and chronic nociceptive behaviors in rats. Daily gabapentin treatment attenuated mechanical allodynia and reduced face-grooming episodes in dIoN-CCI rats. Perspective The orofacial pain caused by trigeminal nerve damage is severe and perhaps more debilitating than other types of neuropathic pain. However, studies on trigeminal neuropathic pain remain limited. This is largely due to the lack of proper animal models given the complexity of the existing surgical procedure required to induce trigeminal nerve injury. Our improved dIoN-CCI model is likely to make it more accessible to study the cellular and molecular mechanisms of neuropathic pain caused by trigeminal nerve damage.

show abstract

“…As a result, various kinds of experimental animal models have been employed to clarify the mechanisms of neuropathic pain, including allodynia, in the trigeminal region. These models involved rats or large animals and were limited to the infraorbital nerve (Benoist et al, 1999;Bird et al, 2002;Elcock et al, 2001;Grelik et al, 2005;Henry et al, 2007;Imamura et al, 1997;Kernisant et al, 2008;Kitagawa et al, 2006;Lim et al, 2007;Long et al, 1998;Vos et al, 1994Vos et al, , 1995. The development of an experimental model involving mice will enable us to provide new insights into the mechanisms of sensory disorders owing to the possibility of using various gene targeting procedures.…”

Section: Introductionmentioning

confidence: 99%

Behavioural and histological observations of sensory impairment caused by tight ligation of the trigeminal nerve in mice

Seino

Seo

Maeda

et al. 2009

Journal of Neuroscience Methods

View full text Add to dashboard Cite

Chronic constriction injury of the infraorbital nerve in the rat using modified syringe needle

Cited by 60 publications

References 19 publications

Inflammatory sensitization of nociceptors depends on activation of NMDA receptors in DRG satellite cells

Inflammatory sensitization of nociceptors depends on activation of NMDA receptors in DRG satellite cells

An Improved Rodent Model of Trigeminal Neuropathic Pain by Unilateral Chronic Constriction Injury of Distal Infraorbital Nerve

Behavioural and histological observations of sensory impairment caused by tight ligation of the trigeminal nerve in mice

Contact Info

Product

Resources

About