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155 The effect of nitric oxide on mechanical and thermal allodynia in neuropathic pain model of rat
Poster Presentations / Animal Models / European Journal of Pain 11(S1) (2007) S59–S207
Z.A. Kamenov *,a,b,d, H. Higashino a, M.K. Todorova c, N. Aoki b, M. Imamura b, V.G. Christov d
S67
b
Department of Physiology, College of Medicine, Kangwon National University, Chuncheon, South Korea
a
Department of Pharmacology, Kinki University School of Medicine, Osaka, Japan b Clinic of Endocrinology, Kinki University School of Medicine, Osaka, Japan c Department of Pathophysiology, Medical University, Sofia, Bulgaria d Clinic of Endocrinology, Medical University, Sofia, Bulgaria Aim. The aim was to differentiate the effects of sucrose loading on thermal pain sensitivity in diabetic and non-diabetic rats. Materials and methods. Five months of age male diabetic Otsuka Long-Evans Tokushima Fatty (OLETF) rats, and their age-matched non-diabetic genetic controls Long Evans Tokusima Otsuka (LETO) rats, were used. The animals were fed with standard laboratory chow and divided into the following four groups: Group O-sucrose (n = 20) – OLETF rats were loaded for 2 months with 30% sucrose in the drinking water (sucrose period). Then the rats were put again on pure tap water (washout period) until the end of the experiment. Group O-control (n = 9) – on tap water in the course of the whole experiment. Group L-sucrose (n = 16) and group L-control (n = 9) – age-matched LETO rats had the same schedule like the groups O-sucrose and O-control, respectively. Sensitivity to noxious thermal stimuli was assessed by the latency time during tail-flick test. The beam was focused on the ventral surface, 5 cm from the tip of the tail. Results. At baseline, at the end of the sucrose period, and 2 moths later (during the washout period), respectively, the groups presented with following latencies (means ± SD): O-sucrose = 6.9 ± 1.4; 7.5 ± 0.9 and 8.4 ± 0.9 (p < 0.5 vs.baseline and vs. O-control); O-control = 7.6 ± 0.6; 7.1 ± 0.7 and 7.2 ± 1.0 (p < 0.5 vs. Lcontrol); L-sucrose = 7.6 ± 1.0; 6.2 ± 1.0 and 5.8 ± 1.4 (p < 0.5 vs. baseline); L-control = 8.4 ± 1.4; 6.0 ± 1.4 and 6.0 ± 0.8 (p < 0.5 vs. baseline). Conclusion. Sucrose loading decreases pain sensitivity, measured with tail-flick test in diabetic, but not in non-diabetic rats. doi:10.1016/j.ejpain.2007.03.169
155 THE EFFECT OF NITRIC OXIDE ON MECHANICAL AND THERMAL ALLODYNIA IN NEUROPATHIC PAIN MODEL OF RAT S.H. Kim *, a, S.J. Jung b a
Department of Neurology, College of Medicine, Kangwon National University, Chuncheon, South Korea
Background. Nitric oxide (NO) is known to play causative role in the development of neuropathic pain following peripheral nerve injury. However, it is yet to be investigated whether the role of NO differs in pain modalities, such as mechanical and thermal stimuli. Also, it has not been investigated whether NO has different roles in the stages of neuro-pathic pain – its development and maintenance. Methods. Neuropathic pain was induced by a resection of the lumbar dorsal root 5, 6 (L 5, 6). After N-nitro-L-arginine methyl ester (L-NAME), an NO synthase inhibitor was injected intrathecally or locally around the dorsal root, we observed the behavioral response to the mechanical and thermal stimuli. Results. Mechanical and thermal allodynia was inhibited by the application of L-NAME before the dorsal root injury. However, L-NAME did not affect the mechanical and thermal allodynia during the maintenance of neuropathic pain. Conclusions. We suggest that NO in the spinal cord or injured perineural site may play an important role in the induction of neuropathic pain, and may be associated with mechanical and thermal allodynia. doi:10.1016/j.ejpain.2007.03.170
156 MODIFICATION OF BURSTING ACTIVITIES IN SOMATOSENSORY CORTEX IN INFLAMEDRATS IN VIVO K. Koga *, H. Shiokawa, M. Mizuno, A. Doi, H. Takase/Mizuguchi, H. Furue, M. Yoshimura Integrative Physiology, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan Aim of investigation. Extracellular recordings have shown that the acute inflammation causes the enhancement of the responsiveness in the primary somatosensory (SI) cortex neurons in rats. However, little is known how the modification in SI contributes to mechanisms of chronic pain following peripheral inflammation. In order to elucidate the mechanisms, the changes in the responsiveness of SI neurons were analyzed in normal and complete freuid ajuband (CFA)inflamed rats in vivo. Methods. CFA was injected into the left hindlimb under pentobarbital anesthesia. Using in vivo patchclamp tequnique, we recorded from layer IV pryramidal neurons of SI receiving inputs from the contralateral hindlimb under urethane anethesisia. Current and voltage clamp were used to analyze the frequency and
Z.A. Kamenov *,a,b,d, H. Higashino a, M.K. Todorova c, N. Aoki b, M. Imamura b, V.G. Christov d
S67
b
Department of Physiology, College of Medicine, Kangwon National University, Chuncheon, South Korea
a
Department of Pharmacology, Kinki University School of Medicine, Osaka, Japan b Clinic of Endocrinology, Kinki University School of Medicine, Osaka, Japan c Department of Pathophysiology, Medical University, Sofia, Bulgaria d Clinic of Endocrinology, Medical University, Sofia, Bulgaria Aim. The aim was to differentiate the effects of sucrose loading on thermal pain sensitivity in diabetic and non-diabetic rats. Materials and methods. Five months of age male diabetic Otsuka Long-Evans Tokushima Fatty (OLETF) rats, and their age-matched non-diabetic genetic controls Long Evans Tokusima Otsuka (LETO) rats, were used. The animals were fed with standard laboratory chow and divided into the following four groups: Group O-sucrose (n = 20) – OLETF rats were loaded for 2 months with 30% sucrose in the drinking water (sucrose period). Then the rats were put again on pure tap water (washout period) until the end of the experiment. Group O-control (n = 9) – on tap water in the course of the whole experiment. Group L-sucrose (n = 16) and group L-control (n = 9) – age-matched LETO rats had the same schedule like the groups O-sucrose and O-control, respectively. Sensitivity to noxious thermal stimuli was assessed by the latency time during tail-flick test. The beam was focused on the ventral surface, 5 cm from the tip of the tail. Results. At baseline, at the end of the sucrose period, and 2 moths later (during the washout period), respectively, the groups presented with following latencies (means ± SD): O-sucrose = 6.9 ± 1.4; 7.5 ± 0.9 and 8.4 ± 0.9 (p < 0.5 vs.baseline and vs. O-control); O-control = 7.6 ± 0.6; 7.1 ± 0.7 and 7.2 ± 1.0 (p < 0.5 vs. Lcontrol); L-sucrose = 7.6 ± 1.0; 6.2 ± 1.0 and 5.8 ± 1.4 (p < 0.5 vs. baseline); L-control = 8.4 ± 1.4; 6.0 ± 1.4 and 6.0 ± 0.8 (p < 0.5 vs. baseline). Conclusion. Sucrose loading decreases pain sensitivity, measured with tail-flick test in diabetic, but not in non-diabetic rats. doi:10.1016/j.ejpain.2007.03.169
155 THE EFFECT OF NITRIC OXIDE ON MECHANICAL AND THERMAL ALLODYNIA IN NEUROPATHIC PAIN MODEL OF RAT S.H. Kim *, a, S.J. Jung b a
Department of Neurology, College of Medicine, Kangwon National University, Chuncheon, South Korea
Background. Nitric oxide (NO) is known to play causative role in the development of neuropathic pain following peripheral nerve injury. However, it is yet to be investigated whether the role of NO differs in pain modalities, such as mechanical and thermal stimuli. Also, it has not been investigated whether NO has different roles in the stages of neuro-pathic pain – its development and maintenance. Methods. Neuropathic pain was induced by a resection of the lumbar dorsal root 5, 6 (L 5, 6). After N-nitro-L-arginine methyl ester (L-NAME), an NO synthase inhibitor was injected intrathecally or locally around the dorsal root, we observed the behavioral response to the mechanical and thermal stimuli. Results. Mechanical and thermal allodynia was inhibited by the application of L-NAME before the dorsal root injury. However, L-NAME did not affect the mechanical and thermal allodynia during the maintenance of neuropathic pain. Conclusions. We suggest that NO in the spinal cord or injured perineural site may play an important role in the induction of neuropathic pain, and may be associated with mechanical and thermal allodynia. doi:10.1016/j.ejpain.2007.03.170
156 MODIFICATION OF BURSTING ACTIVITIES IN SOMATOSENSORY CORTEX IN INFLAMEDRATS IN VIVO K. Koga *, H. Shiokawa, M. Mizuno, A. Doi, H. Takase/Mizuguchi, H. Furue, M. Yoshimura Integrative Physiology, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan Aim of investigation. Extracellular recordings have shown that the acute inflammation causes the enhancement of the responsiveness in the primary somatosensory (SI) cortex neurons in rats. However, little is known how the modification in SI contributes to mechanisms of chronic pain following peripheral inflammation. In order to elucidate the mechanisms, the changes in the responsiveness of SI neurons were analyzed in normal and complete freuid ajuband (CFA)inflamed rats in vivo. Methods. CFA was injected into the left hindlimb under pentobarbital anesthesia. Using in vivo patchclamp tequnique, we recorded from layer IV pryramidal neurons of SI receiving inputs from the contralateral hindlimb under urethane anethesisia. Current and voltage clamp were used to analyze the frequency and