We show that transsynaptic apoptosis is induced in the superficial dorsal horn (laminas I-III) of the spinal cord by three distinct partial peripheral nerve lesions: spared nerve injury, chronic constriction, and spinal nerve ligation. Ongoing activity in primary afferents of the injured nerve and glutamatergic transmission cause a caspase-dependent degeneration of dorsal horn neurons that is slow in onset and persists for several weeks. Four weeks after spared nerve injury, the cumulative loss of dorsal horn neurons, determined by stereological analysis, is Ͼ20%.
We have previously reported a novel method for producing chronic nociceptive behavior in rats following compression of the trigeminal ganglion. In the present study, we have further studied the role of demyelination in the development of prolonged nociceptive behavior in the trigeminal territory. For this purpose, lysophosphatidic acid (LPA) was injected into the trigeminal ganglia of male Sprague-Dawley rats weighing between 250 and 260 g. Under pentobarbital sodium anesthesia, the rats were mounted onto a stereotaxic frame and 3 microL of LPA (1 nmol) solution was injected into the trigeminal ganglion to produce demyelination. This treatment decreased the air-puff thresholds both ipsilateral and contralateral to the injection site, which persisted until postoperative day 100 and returned to the preoperative levels 130 days after the LPA injection. The LPA injection also produced a significant ipsilateral hyper-responsiveness to pin-prick stimulation. The effects of DGPP, an LPA1/3 receptor antagonist, and Y-27632, a Rho kinase inhibitor, upon LPA-induced mechanical allodynia and hyperalgesia were also investigated. Pretreatment with DGPP blocked both mechanical allodynia and ipsilateral hyperalgesia. However, pretreatment with Y-27632 blocked only ipsilateral and contralateral mechanical allodynia. These results thus indicate that a targeted blockade of LPA receptor and Rho kinase pathways are potentially important new treatments for demyelination-induced trigeminal neuralgia-like nociception.
Because the optic disc in myopic eyes is different from a normal optic disc, there are many difficulties in examining the optic discs of myopic eyes. To study optic disc change due to myopia, we performed a morphometrical study of stereophotographs of 61 men, 109 eyes, who had no glaucoma history. The range of refractive error was from +0.75 diopter to -12.75 diopter, and all subjects had intraocular pressure below or equal to 21 mmHg. According to the increase in the myopic degree, the temporal slope of the disc cup was significantly decreased, but the ratio of the vertical disc diameter (VDD) to the horizontal disc diameter and the ratio of the width of peripapillary atrophy (PPA) to the VDD were significantly increased. The above results suggests that in high myopia the optic disc was tilted and the rim-cup border was indistinct and there are some problems in the estimation of the morphometric parameters. Also in evaluation of the PPA of myopic glaucoma patients, there may be some difficulty in deciding whether it is due to myopic change or glaucomatous damage.
Microinjection of formalin (5%, 50 microl) into a temporomandibular joint (TMJ) causes noxious behavioral responses in freely moving rats. In the present study, we investigated the role of central cyclooxygenase (COX) pathways in IL-1beta-induced hyperalgesia with formalin-induced TMJ pain model. Intra-articular injection of 100 pg or 1 ng of IL-1beta significantly facilitated formalin-induced behavior by 130 or 174% in the number of scratches. Intracisternal administration of 100 pg or 1 ng of IL-1beta also significantly increased formalin-induced behavior by 166 or 82% in the number of scratches. IL-1beta-induced hyperalgesia was blocked by pretreatment with IL-1 receptor antagonist. Intracisternal pretreatment with SC-560, a selective COX-1 inhibitor, or NS-398, a selective COX-2 inhibitor, abolished intra-articular administration of IL-1beta-induced hyperalgesic response. Intracisternal pretreatment with NS-398, a selective COX-2 inhibitor, abolished the intracisternal administration of IL-1beta-induced hyperalgesic response, while pretreatment with SC-560, a selective COX-1 inhibitor, did not change IL-1beta-induced hyperalgesic responses. On the other hand, pretreatment with acetaminophen, a tentative COX-3 inhibitor, also abolished both intra-articular and intracisternal administration of IL-1beta-induced hyperalgesic responses. These results indicate that central COX-2 plays important role in the central administration of IL-1beta-induced hyperalgesia and that central COX-1/2 pathways mediate peripheral administration of IL-1beta-induced hyperalgesia in the TMJ. Central COX-3 inhibitor seems to play an important role in the nociceptive process associated with both peripheral and central administration of IL-1beta-induced hyperalgesia in TMJ. It is concluded that central acting of COX-3 inhibitors may be of therapeutic value in the treatment of inflammatory pain in TMJ.
The present study investigated the role of peripheral group I and II metabotropic glutamate receptors (mGluRs) in interleukin-1beta (IL-1beta)-induced mechanical allodynia in the orofacial area. Experiments were carried out on Sprague-Dawley rats weighing between 230 and 280 g. After subcutaneous administration of 0.01, 0.1, 1, or 10 pg of IL-1beta, we examined withdrawal behavioral responses produced by 10 successive trials of a ramp of air-puffs pressure applied ipsilaterally or contralaterally to the IL-1beta injection site. The thresholds of air puffs were measured 10, 30, 60, 120, or 180 min after 25 microl of IL-1beta was administered through an implanted tube. Subcutaneous injection of IL-1beta produced bilateral mechanical allodynia. While the IL-1beta-induced mechanical allodynia was blocked by pretreatment with an IL-1 receptor antagonist, the IL-1beta-induced mirror-image mechanical allodynia was not blocked by an IL-1 receptor antagonist injected into the contralateral side. Subcutaneous administration of CPCCOEt or LY367385, an mGluR1 antagonist, or MPEP or SIB1893, an mGluR5 antagonist, 10 min prior to injection of IL-1beta abolished IL-1beta-induced mechanical allodynia. Pretreatment with APDC or DCG4, a group II mGluR agonist, blocked the IL-1beta-induced mechanical allodynia. The anti-allodynic effect induced by APDC was inhibited by pretreatment with LY341495, a group II mGluR antagonist. These results suggest that peripheral group I and II mGluRs participate in IL-1beta-induced mechanical allodynia in the orofacial area. Peripheral group I mGluR antagonists blocked the IL-1beta-induced mechanical allodynia, while peripheral group II mGluR agonists produced anti-allodynic effects on IL-1beta-induced mechanical allodynia in the orofacial area of rats.
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