Intracisternal administration of mitogen-activated protein kinase inhibitors reduced mechanical allodynia following chronic constriction injury of infraorbital nerve in rats

Lim, Eic Ju; Jeon, Hye Jin; Yang, Gwi Y.; Lee, Min K.; Ju, Jae Kyun; Han, Seung Ro; Ahn, Dong Kuk

doi:10.1016/j.pnpbp.2007.05.016

Cited by 48 publications

(40 citation statements)

References 58 publications

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“…19,20 These animals exhibit mechanical 32,35,48 and cold allodynia 9,18 and heat hyperalgesia. 32 However, to date only 1 study previously tested cold allodynia using acetone applied onto the vibrissal pad skin following infraorbital nerve constriction in rats, 25 and the results did not differ substantially from those reported herein in mice in terms of the time course of the effects observed. As recently reported, 1 the neuropathic mice employed in the present study exhibit a behavioral pattern consistent with the pain that occurs in posttraumatic trigeminal pain patients.…”

Section: Rubbing/scratching Behavior (S) Saline T-3h + Sham Saline T-mentioning

confidence: 69%

Cyclotraxin-B, a New TrkB Antagonist, and Glial Blockade by Propentofylline, Equally Prevent and Reverse Cold Allodynia Induced by BDNF or Partial Infraorbital Nerve Constriction in Mice

Constandil¹,

Goich²,

Hernández³

et al. 2012

The Journal of Pain

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Section: Rubbing/scratching Behavior (S) Saline T-3h + Sham Saline T-mentioning

confidence: 69%

Cyclotraxin-B, a New TrkB Antagonist, and Glial Blockade by Propentofylline, Equally Prevent and Reverse Cold Allodynia Induced by BDNF or Partial Infraorbital Nerve Constriction in Mice

Constandil¹,

Goich²,

Hernández³

et al. 2012

The Journal of Pain

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“…Also in the orofacial area, recent studies have indicated that glial mechanisms contribute to acute and chronic orofacial pain by influencing central sensitization processes in the trigeminal subnucleus caudalis (Vc) 6,7,11,12,25,39,40,42,57,61–63 . These studies also suggest that activation of MAPKs in glial cells is essential in central mechanisms of orofacial pain 15,17,25,30,55,61,64 . In the current study, we tested whether the placement of an occlusal interference induces neuroplastic changes reflecting central sensitization of Vc nociceptive neurons, and whether glial activation and changes in MAPK signaling pathways accompany the trigeminal central sensitization and associated facial hypersensitivity.…”

Section: Introductionmentioning

confidence: 79%

Central Sensitization and MAPKs Are Involved in Occlusal Interference-Induced Facial Pain in Rats

Cao

et al. 2013

The Journal of Pain

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We previously developed a rat dental occlusal interference model of facial pain that was produced by bonding a crown onto the right maxillary first molar and was reflected in sustained facial hypersensitivity that was suggestive of the involvement of central sensitization mechanisms. The aim of the present study was to investigate potential central mechanisms involved in the occlusal interference-induced facial hypersensitivity. A combination of behavioral, immunohistochemical, Western blot and electrophysiological recording procedures was used in 98 male adult Sprague-Dawley rats that either received the occlusal interference or were sham-operated or naive rats. Immunohistochemically labeled astrocytes and microglia in trigeminal subnucleus caudalis (Vc) showed morphological changes indicative of astrocyte and microglial activation after the occlusal interference. Prolonged upregulation of p38 MAPK and ERK was also documented in Vc after placement of the occlusal interference, and was expressed in both neurons and glial cells at time points when rats showed peak mechanical facial hypersensitivity. The i.t. administration of the p38 MAPK inhibitor SB203580 to the medulla significantly inhibited the occlusal interference-induced hypersensitivity, and the ERK inhibitor PD98059 produced an even stronger effect. Central sensitization of functionally identified Vc nociceptive neurons following placement of the occlusal interference was also documented by extracellular electrophysiological recordings, and i.t. administration of PD98059 could reverse the neuronal central sensitization. These novel findings suggest that central mechanisms including central sensitization of trigeminal nociceptive neurons and non-neuronal processes involving MAPKs play significant roles in the production of occlusal interference-induced facial pain. Perspective Central mechanisms including trigeminal nociceptive neuronal sensitization, non-neuronal processes involving glial activation and MAPKs play significant roles in occlusal interference-induced facial pain. These mechanisms may be involved in clinical manifestations of facial pain that have been reported in patients with an occlusal interference.

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“…2). This reduction is not generally reported as most studies begin testing at day 3 post-surgery (Imamura et al, 1997;Kitagawa et al, 2006;Lim et al, 2007) and could be due to residual effects of the anesthetic and analgesics given during surgery or an increase in post-surgical endogenous opioids. Beginning three days after surgery the response score increased and reached a plateau by post-surgery day 5.…”

Section: Behavior -Von Frey Testingmentioning

confidence: 97%

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

Kernisant

Gear

Jasmin

et al. 2008

Journal of Neuroscience Methods

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Here we report a method for performing a chronic constriction injury (CCI) of the infraorbital nerve (ION) in the rat as a component of a chronic pain model. The surgical approach to the ION is described together with the use of a modified dental syringe needle that simplifies placing two chromic gut ligatures around the ION. This method makes the surgical procedure easier, the nerve injury more consistent across animals and reduces secondary damage to the ION and surrounding tissue. Pain behavior testing together with immunostaining for markers of nerve injury in the spinal trigeminal nucleus show the suitability of this procedure as a model of orofacial pain.

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Intracisternal administration of mitogen-activated protein kinase inhibitors reduced mechanical allodynia following chronic constriction injury of infraorbital nerve in rats

Cited by 48 publications

References 58 publications

Cyclotraxin-B, a New TrkB Antagonist, and Glial Blockade by Propentofylline, Equally Prevent and Reverse Cold Allodynia Induced by BDNF or Partial Infraorbital Nerve Constriction in Mice

Cyclotraxin-B, a New TrkB Antagonist, and Glial Blockade by Propentofylline, Equally Prevent and Reverse Cold Allodynia Induced by BDNF or Partial Infraorbital Nerve Constriction in Mice

Central Sensitization and MAPKs Are Involved in Occlusal Interference-Induced Facial Pain in Rats

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

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