BACKGROUND AND OBJECTIVE: Neuropathic pain is a consequence of disease or trauma to peripheral nerves or the central nervous system. In spite of so many people suffering from neuropathic pain it is still extremely difficult to treat. The aim of this study was to examine the cumulative effect of adrenal transplantation and intrathecal injection of histogranin (HN) on pain behavior in neuropathic rats.METHODS: In this experimental research 20 rats were allocated to 2 groups, 10 rats in each. One week after unilateral sciatic nerve ligation using chronic constriction injury (CCI) model, animals received either adrenal medullary or control striated muscle tissue transplantation in lumbar part of spinal cord. One week after animals received different doses of HN (0.5, 1, 3, 6 mg/10ml) or saline interathecally. Behavioral tests were preformed before induction of CCI, before transplantation, before injection and 10 min after injection of HN.FINDINGS: CCI caused heat and MECHANICAL HYPERALGESIA. In adrenal transplanted animals heat and MECHANICAL thresholds in animals which received low dose of histogranin (0.5 mg/kg) was 9.3±0.6 and 9.5±1.1, respectively which increased comparing to before injection time (p<0.05). Injection of 6 mg HN was not effective. In muscle transplanted animal’s only higher dose of histogranin increase thermal threshold. Thermal threshold in this groups increased from 6.4±0.35 before injection time to 9±0.9 after injection of 3 mg of HN (p<0.05). However alleviation of pain was significant with the lower doses of histogranin in adrenal medullary transplanted animals (p<0.05).CONCLUSION: The results showed that the pain alleviation effect of histogranin when accompained with adrenal medullary graft is dose dependant and low doses of histogranin can augment the effects of adrenal medullary transplants and may be an effective adjunct in the treatment of chronic pain.

Aim and Background: Pain is one of the factors that produce after of decrease or opiates stop. The purpose of this study was to determination the effect of exercise training on evoking of Hypoalgesia effect subsequent of increased BEND levels in the addicts.Methods and Materials: In this study, 20 male addicts (20-33 years old) were selected after public call and divided into drug supplement (N=10) and exercise -drug supplement (N=10) groups. The first group was performed exercise training to intensity of 70-75 percent of VO2max for twenty sessions (5 sessions per week and for 45 to 55 minutes in each session). They also was consumption 10 milligrams Methadone. The second group only was consumption 10 milligrams methadone daily. After it we survey b- Endorphin levels and hypoalgesia due to MECHANICAL pain and pain due to decrease and increase of temperature.Findings: Statistic analysis was shown that the amounts of BEND significantly increase in both groups (P<0.05). Also, the first group significantly enhanced status of hypoalgesia in all of painful stimulus (P<0.05). Conclusions: Presumably method of exercise-drug supplement is better for decrease and management of pain in addicts.

The use of multiple loose ligations of the rat sciatic nerve has been proposed as a model for the study of allodynia and HYPERALGESIA. This pain hypersensitivity results from both an increase in the peripheral and central sensitization. The evidence indicating that the development of neuropathic thermal HYPERALGESIA and MECHANICAL allodynia requires activation of spinal cord NMDA receptors. NMDA antagonists are capable of blocking central sensitization associated with persistent noxious stimulation in experimental mononeuropathy and opioid tolerance. In addition, it has been reported that treatment with MK801 prevents the thermal HYPERALGESIA and MECHANICAL allodynia. In the present study we attempted to find the interaction of NMAD receptor antagonist MK801 and opioid receptor agonist morphine in two nerve injury models of neuropathic pain in attenuation of HYPERALGESIA and allodynia. The experiments were carried out on male Sprauge-Dawley rats weighing 200-250 g. Under anesthesia, the sciatic nerve were exposed unilaterally and ligated loosely with 4-0 chromic gut. In SNI procedure axotomy and ligation of tibial and common peroneal nerves, leaving the sural nerve intact. We observed that pretreatment with NMDA recepor antagonist MK801 (0.3 mg/kg) does significantly attenuated thermal HYPERALGESIA and MECHANICAL allodynia.in both SNI and CCI. Preemptive injection of morphine (8 mg/kg) had to a much lesser than MK801 in HYPERALGESIA and allodynia in SNI and CCI models. Co-administration of morphine and MK801 could eliminate the hyperesthetic and allodynia state following sciatic nerve injury. In conclusion, the present study shows that the opioids alone could actually contribute to the development of neuronal plastic changes via interactions with NMDA receptors. Then morphine during the preoperative period in rats failed to affect the development of post-operative HYPERALGESIA and allodynia.

Introduction: Glial activation and secretion of cytokines at the spinal level is known as part of chronic pain pathogenesis. Although changes in TNFa at the supraspinal level are reported during chronic pain, its exact role and site of action remain to be elucidated. We investigated the effect of microinfusion of TNFa into the LC in a rat model of neuropathic pain.Methods: Male Wistar rats were cannulated in the LC. The cannula was connected to an Alzet mini-osmotic pump, which was filled by the drug (vehicle, TNFa or TNFa-antibody) and placed subcutaneously behind the neck. Twenty four-48 hours after cannulation, a chronic constriction injury (CCI) surgery was performed on the contralateral sciatic nerve. HYPERALGESIA and allodynia symptoms were assessed 2, 4, 6, 8, 10 and 12 days after CCI.Results: Microinfusion of TNFa (100ng/day) into the LC significantly exacerbated the HYPERALGESIA in rat models of neuropathic pain on days 2 and 8 after CCI. On the other hand, microinfusion of TNFa antibody (250ng/day) decreased the symptoms of HYPERALGESIA on days 2, 4, 6, 8, 10 and 14. TNFa antibody also significantly alleviated the CCIinduced allodynia.Conclusion: These data suggest that alterations of TNFa levels in the LC play a crucial role in the development and maintenance of neuropathic pain.

Objective: von Frey Filament (vFF) is an aesthesiometer to measure paw withdrawal thresholds. Our aim was to validate the manually von Frey test technique for assessing neuropathic pain behavioral signs in a sciatic nerve ligation model. Materials and Methods: In this experimental study, peripheral neuropathic pain associated with sciatic nerve chronic ligation (SN-CL) was induced. Filaments used against posterior pad mid-plantar region using a simplified up-down method (SUDO). In addition to baseline withdrawal thresholds, the behavioral test was repeated after surgery thrice more with an interval of ten days. vFF (2 to 26 g) were used in ascending order for HYPERALGESIA assessment. Results: In SN-CL rats, the results validate a loss of pain sensation, resulted in, long-lasting ipsilateral allodynia with the development of contralateral allodynia later and an extraterritorial development of neuropathic signs. Variability for the development of ipsilateral and contralateral allodynia over time was noted in sham (SH) control rats. SN-CL group showed a contralateral HYPERALGESIA development just at the 16th-day after surgery with an absence of ipsilateral HYPERALGESIA development at the different days of paw withdrawal thresholds measurements. Conclusion: Manually vFF test technique was successfully used for assessing neuropathic pain behavioral signs in sciatic a nerve ligation model with the absence of ipsilateral HYPERALGESIA development.

Background: Neuropathic pain arising from sciatic nerve ligation (SNL) injury can result in increased sensitivity to both noxious (HYPERALGESIA) and non-noxious stimuli (allodynia). Some research studies have been shown that the mechanisms underlying neuropathic pain processing differed as a function of gender and gonadal hormone status. In this study, we try to show the effects of nerve injury after gonadectomy in time-course of HYPERALGESIA that has not been extensively studied.Methods and Materials: 45 albino male mice weighting 25-35 gr were subjected to Intact, Shamoperated, Sciatic Nerve Ligated, Gonadectomized, and Sciatic Nerve Ligated+Gonadectomized groups. The tail flick latency was measured at set intervals 10th-20th days for 11 days after surgical operation (peripheral nerve injury by left sciatic nerve ligation and gonadectomy) in all groups by tail flick analgesiometer.Results: The gonadectomizedmice responded (7.15±1.8 sec) significantly faster than intact ones (10.78±1.43 sec) to a thermal nociceptive stimulus (P<0.05). In ligated mice, HYPERALGESIA developed significantly within 11-17 days after sciatic nerve ligation (6.35±1.33 sec; P<0.05). In sciatic nerve ligated+gonadectomized group, tail flick latency time (5.45±1.14 sec) decreased significantly within 11 and 13-16 days after surgical operations in comparison with sham-operated mice (9.99±1.64 sec; P<0.05) and as compared with tail flick latency in sciatic nerve ligated mice (6.62±1.75 sec) within 13th-14th (P<0.05) and 15th (P<0.01) days after surgical operations.Conclusions: It was concluded that testosterone might play a role in the pain modulation. In addition, we suggest that testosterone also affects neuropathic pain that is accompanied by a number of neuroplastic alternations at the level of spinal cord including up- and down-regulation of neurotransmitters during sciatic nerve ligation-induced HYPERALGESIA.