The present study was performed to investigate the modulatory role of certain interleukin (IL)-1β in nociception with a nociceptive jaw opening reflex and an orofacial formalin test in freely moving rats. In an acute pain model, 10 pg, 100 pg and 1 ng IL-1β injected intracisternally did not change the digastric eletromyogram (dEMG). However, 10 ng IL-1β suppressed dEMG to 76±8 % of control values. In an inflammatory pain model, 10 pg IL-1β injected intracisternally did not change formalin-induced noxious behavioral responses. However, 100 pg IL-1β increased formalin-induced noxious behavioral responses. At higher dose of 10 ng IL-1β, it did not increase formalin-induced behavioral responses. Pretreatment with IL-1 receptor antagonist abolished hyperalgesic response of 100 pg IL-1β. These results suggest that the intracisternal injection of IL-1β modulate the transmission of nociceptive information in the orofacial area. The hypo/hyper-algesic responses of central cytokines seem to depend on the pain model or dose related manner and the hyperalgesic action seems to be mediated by IL-1 receptor.
本研究以自由运动大鼠为实验对象，通过伤害性张开颌反射和口面部福尔马林试验，探讨某些白细胞介素-1β在伤害性中的调节作用。在急性疼痛模型中，腹腔注射10 pg、100 pg和1 ng IL-1β均未改变二腹肌电图(dEMG)。然而，10 ng IL-1β抑制dEMG至控制值的76±8%。在炎症性疼痛模型中，腹腔注射10 pg IL-1β不会改变福尔马林诱导的有害行为反应。然而，100 pg IL-1β增加了福尔马林诱导的有害行为反应。在高剂量10 ng IL-1β时，不增加福尔马林诱导的行为反应。IL-1受体拮抗剂预处理可消除100pg IL-1β的过敏反应。这些结果表明，内胆注射IL-1β可调节口面区伤害性信息的传递。中枢细胞因子的低/高痛觉反应似乎依赖于疼痛模型或剂量相关方式，高痛觉作用似乎是由IL-1受体介导的。
{"title":"Differential responses of intracisternal injection of interleukin‐1 β to acute and inflammatory orofacial pain model in freely moving rats","authors":"H. Choi, J. S. Park, D. Ahn","doi":"10.1002/NRC.10047","DOIUrl":"https://doi.org/10.1002/NRC.10047","url":null,"abstract":"The present study was performed to investigate the modulatory role of certain interleukin (IL)-1β in nociception with a nociceptive jaw opening reflex and an orofacial formalin test in freely moving rats. In an acute pain model, 10 pg, 100 pg and 1 ng IL-1β injected intracisternally did not change the digastric eletromyogram (dEMG). However, 10 ng IL-1β suppressed dEMG to 76±8 % of control values. In an inflammatory pain model, 10 pg IL-1β injected intracisternally did not change formalin-induced noxious behavioral responses. However, 100 pg IL-1β increased formalin-induced noxious behavioral responses. At higher dose of 10 ng IL-1β, it did not increase formalin-induced behavioral responses. Pretreatment with IL-1 receptor antagonist abolished hyperalgesic response of 100 pg IL-1β. These results suggest that the intracisternal injection of IL-1β modulate the transmission of nociceptive information in the orofacial area. The hypo/hyper-algesic responses of central cytokines seem to depend on the pain model or dose related manner and the hyperalgesic action seems to be mediated by IL-1 receptor.","PeriodicalId":19198,"journal":{"name":"Neuroscience Research Communications","volume":"43 1","pages":"145-154"},"PeriodicalIF":0.0,"publicationDate":"2002-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"80780023","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Stimulation of the calcium-stimulated and magnesium-dependent adenosine triphosphatase (Ca2+/Mg2+-ATPase) activity by 3-5-3′-L-triiodothyronine (T3) in synaptosomes prepared from adult rat cerebral cortex was demonstrated both in vitro and in vivo. T3 stimulated the Ca2+/Mg2+-ATPase activity in time dependent and dose dependent manner to depolarization-induced synaptosomes suspended in Ca2+-loaded choline-chloride buffer, represented involvement of the recovery phase of the changes in intrasynaptosomal Ca2+ level in this activation. T3 (100nM) also stimulated the enzyme activity in nondepolarized intact synaptosomes suspended in choline-chloride buffer. T3 had direct and dose-dependent stimulatory effect on the Ca2+/Mg2+-ATPase activity of the lysed synaptosomal suspension. The effect of T3 on the lysed synaptosomes was higher than that found on the nondepolarized intact synaptosomes. The condition probably represents the direct and/or indirect interaction of T3 with the enzyme through plasmamembrane related phenomenon that needs further investigation. After T3 treatment, a dose-dependent activation of the enzyme was found in vivo. It appears that T3 plays a role on adult brain neuronal Ca2+-mobilization through stimulation of the Ca2+/Mg2+-ATPase activity in nerve terminals.
体外和体内实验证实了3-5-3′- l -三碘甲状腺原氨酸(T3)对成年大鼠大脑皮层突触体钙刺激和镁依赖的腺苷三磷酸酶(Ca2+/Mg2+- atp酶)活性的刺激作用。T3以时间依赖和剂量依赖的方式刺激Ca2+/Mg2+- atp酶活性，以去极化诱导的突触体悬浮在Ca2+负载的氯化胆碱缓冲液中，代表了这种激活中突触体内Ca2+水平变化的恢复阶段的参与。T3 (100nM)也刺激悬于氯化胆碱缓冲液中的未去极化完整突触体的酶活性。T3对裂解的突触体悬浮液的Ca2+/Mg2+- atp酶活性有直接和剂量依赖性的刺激作用。T3对裂解的突触体的影响高于未去极化的完整突触体。这种情况可能是T3通过质膜与酶直接或间接相互作用的结果，需要进一步研究。在T3治疗后，体内发现了一种剂量依赖性的酶激活。似乎T3通过刺激神经末梢Ca2+/Mg2+- atp酶活性，在成人脑神经细胞Ca2+动员中起作用。
{"title":"Stimulation of Ca2+/Mg2+‐ATPase activity in adult rat cerebrocortical synaptosomes by 3‐5‐3′‐L‐triiodothyronine","authors":"Nilkanta Chakrabarti, A. Ray","doi":"10.1002/NRC.10052","DOIUrl":"https://doi.org/10.1002/NRC.10052","url":null,"abstract":"Stimulation of the calcium-stimulated and magnesium-dependent adenosine triphosphatase (Ca2+/Mg2+-ATPase) activity by 3-5-3′-L-triiodothyronine (T3) in synaptosomes prepared from adult rat cerebral cortex was demonstrated both in vitro and in vivo. T3 stimulated the Ca2+/Mg2+-ATPase activity in time dependent and dose dependent manner to depolarization-induced synaptosomes suspended in Ca2+-loaded choline-chloride buffer, represented involvement of the recovery phase of the changes in intrasynaptosomal Ca2+ level in this activation. T3 (100nM) also stimulated the enzyme activity in nondepolarized intact synaptosomes suspended in choline-chloride buffer. T3 had direct and dose-dependent stimulatory effect on the Ca2+/Mg2+-ATPase activity of the lysed synaptosomal suspension. The effect of T3 on the lysed synaptosomes was higher than that found on the nondepolarized intact synaptosomes. The condition probably represents the direct and/or indirect interaction of T3 with the enzyme through plasmamembrane related phenomenon that needs further investigation. After T3 treatment, a dose-dependent activation of the enzyme was found in vivo. It appears that T3 plays a role on adult brain neuronal Ca2+-mobilization through stimulation of the Ca2+/Mg2+-ATPase activity in nerve terminals.","PeriodicalId":19198,"journal":{"name":"Neuroscience Research Communications","volume":"32 1","pages":"193-201"},"PeriodicalIF":0.0,"publicationDate":"2002-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"91352329","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
T. Kurt, A. Oğuzhanoğlu, R. Ortaç, B. Turman, E. Adiguzel
We investigated whether administration of L-arginine reduces the ischaemia-reperfusion damage in the rat brain. The effects of L-arginine were evaluated by means of somatosensory evoked potential (SEP) measurements and quantitative histopathological investigations. There was no significant difference between groups based on SEP data. The results obtained from quantitative histopathological investigations indicate that the nitric oxide (NO) precursor L-arginine does not appear to have a protective effect on the brain ischaemia-reperfusion damage. Furthermore, histopathological evaluation revealed a higher number of damaged cells in the L-arginine treated rats than in control group. The results of the present study suggest that high concentrations of L-arginine present in later stages of reperfusion might have harmful effects on reperfusion damage in the brain.
{"title":"Effects of L‐arginine on the brain ischaemia‐reperfusion damage in rats: An investigation by somatosensory evoked potentials and histopathology","authors":"T. Kurt, A. Oğuzhanoğlu, R. Ortaç, B. Turman, E. Adiguzel","doi":"10.1002/NRC.10050","DOIUrl":"https://doi.org/10.1002/NRC.10050","url":null,"abstract":"We investigated whether administration of L-arginine reduces the ischaemia-reperfusion damage in the rat brain. The effects of L-arginine were evaluated by means of somatosensory evoked potential (SEP) measurements and quantitative histopathological investigations. There was no significant difference between groups based on SEP data. The results obtained from quantitative histopathological investigations indicate that the nitric oxide (NO) precursor L-arginine does not appear to have a protective effect on the brain ischaemia-reperfusion damage. Furthermore, histopathological evaluation revealed a higher number of damaged cells in the L-arginine treated rats than in control group. The results of the present study suggest that high concentrations of L-arginine present in later stages of reperfusion might have harmful effects on reperfusion damage in the brain.","PeriodicalId":19198,"journal":{"name":"Neuroscience Research Communications","volume":"9 1","pages":"175-182"},"PeriodicalIF":0.0,"publicationDate":"2002-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"83429055","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Attempts have been made to dissociate the cognitive effects of scopolamine from its non-cognitive effects. It has been suggested that low doses of scopolamine may induce memory impairment without inducing significant non-cognitive effects. We therefore tested changes in locomotor activity (as a non-cognitive effect) in rats treated with low-dose scopolamine (which is believed to induce cognitive effects only). In this study, locomotor activity (as a non-cognitive effect) induced by low doses of this drug was evaluated by using two methods and rat strains. In the first study (circular box method, an automated open-field), scopolamine hydrobromide (HBr), scopolamine methylbromide (MeBr) or saline was injected subcutaneously into male Sprague-Dawley rats. After 30 min, rats were put into an automated open-field and locomotor activity was quantified by recording interruptions of infrared beams, with print-outs every 2 min for 16 min. Locomotor activity was assessed by summing these recordings. In the second study (closed platform), scopolamine HBr or saline was injected intraperitoneally into male Long-Evans rats. Twenty minutes later, the rats were placed in the center of a square-shaped closed platform (with 3×3 divisions). Locomotor activity was defined as the sum of crossings (traversing of four paws of the rat from one area into another of nine) and rears, which were recorded every 5 min for 20 min. Results from the circular box study showed that scopolamine HBr produced a marked increase in locomotor activity whereas scopolamine MeBr produced a non-significant decrease in locomotor activity. The closed platform data also demonstrated that scopolamine HBr increased locomotor activity significantly. These data show that scopolamine can induce non-cognitive effects (such as increased locomotor activity), even at low doses. Our results also imply that the increase in locomotor activity is mediated centrally.
{"title":"Effects of low‐dose scopolamine on locomotor activity: No dissociation between cognitive and non‐effects","authors":"G. Poorheidari, J. Pratt, Nima Dehghani","doi":"10.1002/NRC.10049","DOIUrl":"https://doi.org/10.1002/NRC.10049","url":null,"abstract":"Attempts have been made to dissociate the cognitive effects of scopolamine from its non-cognitive effects. It has been suggested that low doses of scopolamine may induce memory impairment without inducing significant non-cognitive effects. We therefore tested changes in locomotor activity (as a non-cognitive effect) in rats treated with low-dose scopolamine (which is believed to induce cognitive effects only). \u0000 \u0000 \u0000 \u0000In this study, locomotor activity (as a non-cognitive effect) induced by low doses of this drug was evaluated by using two methods and rat strains. In the first study (circular box method, an automated open-field), scopolamine hydrobromide (HBr), scopolamine methylbromide (MeBr) or saline was injected subcutaneously into male Sprague-Dawley rats. After 30 min, rats were put into an automated open-field and locomotor activity was quantified by recording interruptions of infrared beams, with print-outs every 2 min for 16 min. Locomotor activity was assessed by summing these recordings. In the second study (closed platform), scopolamine HBr or saline was injected intraperitoneally into male Long-Evans rats. Twenty minutes later, the rats were placed in the center of a square-shaped closed platform (with 3×3 divisions). Locomotor activity was defined as the sum of crossings (traversing of four paws of the rat from one area into another of nine) and rears, which were recorded every 5 min for 20 min. \u0000 \u0000 \u0000 \u0000Results from the circular box study showed that scopolamine HBr produced a marked increase in locomotor activity whereas scopolamine MeBr produced a non-significant decrease in locomotor activity. The closed platform data also demonstrated that scopolamine HBr increased locomotor activity significantly. \u0000 \u0000 \u0000 \u0000These data show that scopolamine can induce non-cognitive effects (such as increased locomotor activity), even at low doses. Our results also imply that the increase in locomotor activity is mediated centrally.","PeriodicalId":19198,"journal":{"name":"Neuroscience Research Communications","volume":"37 4","pages":"165-174"},"PeriodicalIF":0.0,"publicationDate":"2002-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"91535637","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
In a rat model of spinal cord compression-induced injury, we have tested the hypothesis that intrathecally administered methylprednisolone will improve long-term recovery of the injured rats. The effect of the treatment was evaluated quantitatively as 1, behavioral testing of spontaneous locomotion and 2, morphometric measurement of the tissue loss in the white matter and grey matter, respectively. Intrathecal methylprednisolone elicited remarkable motor reactions in the paraplegic animals immediately after administration. However, during 4 weeks' survival, no significant differences were observed in the parameters of recovery between the methylprednisolone-treated and placebo-treated group. We conclude that intrathecal administration of methylprednisolone had no effect on the outcome after compressive spinal cord injury in the rat at the doses and timing used in the present study.
{"title":"Intrathecal methylprednisolone does not improve outcome after severe spinal cord injury in the rat","authors":"I. Vanický, L. Urdzikova, K. Saganová, M. Marsala","doi":"10.1002/NRC.10051","DOIUrl":"https://doi.org/10.1002/NRC.10051","url":null,"abstract":"In a rat model of spinal cord compression-induced injury, we have tested the hypothesis that intrathecally administered methylprednisolone will improve long-term recovery of the injured rats. The effect of the treatment was evaluated quantitatively as 1, behavioral testing of spontaneous locomotion and 2, morphometric measurement of the tissue loss in the white matter and grey matter, respectively. Intrathecal methylprednisolone elicited remarkable motor reactions in the paraplegic animals immediately after administration. However, during 4 weeks' survival, no significant differences were observed in the parameters of recovery between the methylprednisolone-treated and placebo-treated group. We conclude that intrathecal administration of methylprednisolone had no effect on the outcome after compressive spinal cord injury in the rat at the doses and timing used in the present study.","PeriodicalId":19198,"journal":{"name":"Neuroscience Research Communications","volume":"26 1","pages":"183-191"},"PeriodicalIF":0.0,"publicationDate":"2002-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"83258136","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Yi Li, X. Yang, Jieli Chen, Lei Wang, Ying Wang, Chunling Zhang, Xiaoguang Chen, M. Katakowski, T. Mikkelsen, Mei Lu, M. Chopp
We constructed a biologic material composed of fetal rat brain cells (neurospheres) and adult rat bone marrow stromal cells (MSCs), designated as NMCspheres. Adult rats were subjected to 2 hours of middle cerebral artery occlusion (MCAo) and implanted with cultured prelabeled NMCspheres (n=6), neurospheres (n=5) or MSCs (n=6) into the ischemic penumbra at 24 hours after MCAo. Control adult rats (n=10) were subjected to MCAo alone. In vitro within the NMCspheres, MSCs rapidly formed a process network with intact neural cells compared with a necrotic core within neurospheres alone. An in vivo rat corneal assay demonstrated that NMCspheres enhanced angiogenesis compared to MSCs and neurospheres. Neurological functional recovery after stroke was enhanced in rats treated with NMCspheres, compared to rats with neurosphere or MSC treatments by day 7 and day 14 after transplantation. The NMCspheres are a new composite material that may be employed in the treatment of stroke.
{"title":"Transplantation of a new composite of neural cells and marrow stromal cells into rat brain after stroke","authors":"Yi Li, X. Yang, Jieli Chen, Lei Wang, Ying Wang, Chunling Zhang, Xiaoguang Chen, M. Katakowski, T. Mikkelsen, Mei Lu, M. Chopp","doi":"10.1002/NRC.10048","DOIUrl":"https://doi.org/10.1002/NRC.10048","url":null,"abstract":"We constructed a biologic material composed of fetal rat brain cells (neurospheres) and adult rat bone marrow stromal cells (MSCs), designated as NMCspheres. Adult rats were subjected to 2 hours of middle cerebral artery occlusion (MCAo) and implanted with cultured prelabeled NMCspheres (n=6), neurospheres (n=5) or MSCs (n=6) into the ischemic penumbra at 24 hours after MCAo. Control adult rats (n=10) were subjected to MCAo alone. In vitro within the NMCspheres, MSCs rapidly formed a process network with intact neural cells compared with a necrotic core within neurospheres alone. An in vivo rat corneal assay demonstrated that NMCspheres enhanced angiogenesis compared to MSCs and neurospheres. Neurological functional recovery after stroke was enhanced in rats treated with NMCspheres, compared to rats with neurosphere or MSC treatments by day 7 and day 14 after transplantation. The NMCspheres are a new composite material that may be employed in the treatment of stroke.","PeriodicalId":19198,"journal":{"name":"Neuroscience Research Communications","volume":"115 1","pages":"155-163"},"PeriodicalIF":0.0,"publicationDate":"2002-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"79107877","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Central glucose availability is a critical monitored variable in the regulation of reproductive neuroendocrine function. While current studies implicate the periventricular caudal brainstem as a source of signaling of decreased availability of catabolic intermediates and/or glycolytic end products, the mechanisms by which local metabolic ‘sensors’ signal diminished glucose utilization are not clear. The present experiments investigated whether fourth ventricular infusion of the aerobic catabolic substrate, lactate, attenuates glucoprivic suppression of luteinizing hormone (LH). Cyclic female rats were injected at 13.00h on proestrus with the glucose antimetabolite, 2-deoxy-D-glucose (2DG; 50 vs. 150ug), or vehicle into the rostral fourth ventricle. Additional proestrus animals were treated by continuous fourth ventricular infusion of 10.0 µM lactate/hr or vehicle, initiated prior to ip injection of 400mg 2DG/kg bw or saline. Serial blood samples were obtained hourly during proestrus afternoon for radioimmunoassay of plasma LH. The results demonstrate a reduction in the LH surge following icv 2DG administration, while showing that fourth ventricular infusion of lactate reversed inhibition of hormone release by systemic antimetabolite administration. These findings support the view that hindbrain signaling of glucose metabolic dysfunction initiates neural mechanisms that inhibit the proestrus LH surge, and that lactate utilization may be monitored as an indicator of local cellular energy stasis.
中枢葡萄糖可用性是生殖神经内分泌功能调节的关键监测变量。虽然目前的研究暗示脑室周围尾侧脑干是分解代谢中间体和/或糖酵解终产物可用性降低的信号来源，但局部代谢“传感器”信号减少葡萄糖利用的机制尚不清楚。本实验探讨了第四心室输注有氧分解代谢底物乳酸是否会减弱葡萄糖对黄体生成素(LH)的抑制作用。循环雌性大鼠于发情前13.00h注射葡萄糖抗代谢物2-脱氧-d -葡萄糖(2DG;50 vs 150ug)，或载体进入吻侧第四脑室。其他发情前期动物连续第四心室输注10.0µM乳酸/小时或对照物，在ip注射400mg 2DG/kg bw或生理盐水之前开始。在发情前的下午每小时采集一次连续血液样本，用于血浆LH的放射免疫测定。结果表明，icv - 2DG给药后LH激增减少，同时显示第四心室输注乳酸逆转了全身抗代谢物给药对激素释放的抑制。这些发现支持了以下观点:葡萄糖代谢功能障碍的后脑信号启动了抑制发情前LH激增的神经机制，并且乳酸利用可能被监测为局部细胞能量停滞的一个指标。
{"title":"Hindbrain glucoprivic inhibition of the proestrus lutenizing hormone surge in the female rat is attenuated by exogenous lactate administration","authors":"K. Briski","doi":"10.1002/NRC.10039","DOIUrl":"https://doi.org/10.1002/NRC.10039","url":null,"abstract":"Central glucose availability is a critical monitored variable in the regulation of reproductive neuroendocrine function. While current studies implicate the periventricular caudal brainstem as a source of signaling of decreased availability of catabolic intermediates and/or glycolytic end products, the mechanisms by which local metabolic ‘sensors’ signal diminished glucose utilization are not clear. The present experiments investigated whether fourth ventricular infusion of the aerobic catabolic substrate, lactate, attenuates glucoprivic suppression of luteinizing hormone (LH). Cyclic female rats were injected at 13.00h on proestrus with the glucose antimetabolite, 2-deoxy-D-glucose (2DG; 50 vs. 150ug), or vehicle into the rostral fourth ventricle. Additional proestrus animals were treated by continuous fourth ventricular infusion of 10.0 µM lactate/hr or vehicle, initiated prior to ip injection of 400mg 2DG/kg bw or saline. Serial blood samples were obtained hourly during proestrus afternoon for radioimmunoassay of plasma LH. The results demonstrate a reduction in the LH surge following icv 2DG administration, while showing that fourth ventricular infusion of lactate reversed inhibition of hormone release by systemic antimetabolite administration. These findings support the view that hindbrain signaling of glucose metabolic dysfunction initiates neural mechanisms that inhibit the proestrus LH surge, and that lactate utilization may be monitored as an indicator of local cellular energy stasis.","PeriodicalId":19198,"journal":{"name":"Neuroscience Research Communications","volume":"10 1","pages":"67-73"},"PeriodicalIF":0.0,"publicationDate":"2002-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"85943767","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
L. Rodella, G. Bonaspetti, R. Rezzani, E. Borsani, R. Fenu, U. Pazzaglia, R. Bianchi
When an adult skeletal muscle is denervated, its end-plates degenerate and their acethylcholinesterase (AChE) activity gradually decreases. However, if the proximal segment of the nerve is sutured to the distal segment, or if the nerve is implanted in a previous denerved muscle the axons regenerate and reconstitute new end-plates over a variable period. This period depends on the time passed between the nerve cutting and the reimplantation suggesting that the degenerative processes are closely correlated to regeneration. It has been shown that cyclosporine-A (CsA) is useful in nerve regeneration but their role in nerve degeneration is not well understand. We evaluated, using AChE histochemistry, the effects of CsA, on the degeneration of the end-plates in an experimental model of gastrocnemius muscle denervation in the rat. CsA at a dose of 15 mg/kg/day did not cause any quantitative or qualitative alterations in the end-plates on normal rat muscles. Moreover, our findings showed that CsA reduced the end-plate degeneration and loss in the denerved rat muscles.
当成人骨骼肌失神经时，其终板退行性变，其乙酰胆碱酯酶(AChE)活性逐渐降低。然而，如果将神经近端段与远端段缝合，或者将神经植入以前的无神经肌肉中，轴突会在不同的时间内再生并重建新的终板。这段时间取决于神经切割和再植之间的时间，这表明退行性过程与再生密切相关。环孢素- a (CsA)在神经再生中有重要作用，但在神经退行性变中的作用尚不清楚。我们用乙酰胆碱酯酶组织化学方法评估了CsA对大鼠腓肠肌去神经支配实验模型终板退变的影响。15 mg/kg/天剂量的CsA未引起正常大鼠肌肉终板的定量或定性改变。此外，我们的研究结果表明，CsA减少了大鼠无神经肌肉的终板退变和损失。
{"title":"Cyclosporine‐A delays the end‐plate degeneration in denerved rat muscles","authors":"L. Rodella, G. Bonaspetti, R. Rezzani, E. Borsani, R. Fenu, U. Pazzaglia, R. Bianchi","doi":"10.1002/NRC.10041","DOIUrl":"https://doi.org/10.1002/NRC.10041","url":null,"abstract":"When an adult skeletal muscle is denervated, its end-plates degenerate and their acethylcholinesterase (AChE) activity gradually decreases. However, if the proximal segment of the nerve is sutured to the distal segment, or if the nerve is implanted in a previous denerved muscle the axons regenerate and reconstitute new end-plates over a variable period. This period depends on the time passed between the nerve cutting and the reimplantation suggesting that the degenerative processes are closely correlated to regeneration. It has been shown that cyclosporine-A (CsA) is useful in nerve regeneration but their role in nerve degeneration is not well understand. We evaluated, using AChE histochemistry, the effects of CsA, on the degeneration of the end-plates in an experimental model of gastrocnemius muscle denervation in the rat. CsA at a dose of 15 mg/kg/day did not cause any quantitative or qualitative alterations in the end-plates on normal rat muscles. Moreover, our findings showed that CsA reduced the end-plate degeneration and loss in the denerved rat muscles.","PeriodicalId":19198,"journal":{"name":"Neuroscience Research Communications","volume":"142 1","pages":"85-92"},"PeriodicalIF":0.0,"publicationDate":"2002-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"88669140","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Keyue Ding, Xiaojing Sun, Min Zhou, Jing Cai, Tianjing Cai, Yan Zhang, Tongbin Zhu, Zhengguo Zhang, B. Qiang, Yan Shen
We presented a procedure to identify novel protein-coding genes from human fetal hippocampus ESTs database generated in our previous study. The protocol is involved in searching the GenBank non-redundant (nr) protein database with ESTs coding regions query. We used ESTScan program to detect and reconstruct coding regions in the ESTs sequence data. With almost 10,000 raw ESTs analyzed, 4,061 coding regions were extracted. The corresponding amino acid sequences were then searched against the GenBank nr-protein databases; all the similarity hits were parsed in a homology analysis workbench. 22 ESTs were identified as the “seed” ESTs, which might be the fragment of the novel protein-coding genes. Indeed, further analysis of these ESTs in full-length cDNA cloning in silico, as well as the mapping information in UCSC and the added experimental proof, verified the effectiveness of the strategy. Taking advantage of rare ESTs resources, and the effective strategy, we would explore more novel genes in the human genome. [The ESTs sequence data described in this paper have been submitted to the GenBank data library (http://www.ncbi.nlm.nih.gov/dbEST) under accession nos. BM174886-958, BM259607-9; and the full length cDNA sequence can be obtained in http://www.chgb.org.cn/hippocampus.htm]
我们提出了一种从我们以前的研究中产生的人类胎儿海马ESTs数据库中鉴定新的蛋白质编码基因的方法。该协议涉及到对GenBank非冗余(nr)蛋白数据库进行ESTs编码区域查询。利用ESTScan程序对ESTs序列数据中的编码区域进行检测和重构。在分析了近10,000个原始ESTs后，提取了4,061个编码区域。然后在GenBank nr-protein数据库中检索相应的氨基酸序列;所有相似点都在同源性分析工作台中进行解析。22条est被鉴定为“种子”est，可能是新蛋白编码基因的片段。事实上，通过对这些est的芯片全长cDNA克隆的进一步分析，以及UCSC中的定位信息和增加的实验证明，验证了该策略的有效性。利用稀缺的est资源和有效的策略，我们将在人类基因组中探索更多的新基因。[本文中描述的ESTs序列数据已提交至GenBank数据库(http://www.ncbi.nlm.nih.gov/dbEST)， accession no . BM174886-958, BM259607-9;全长cDNA序列可从http://www.chgb.org.cn/hippocampus.htm获取]
{"title":"Identification of novel protein-coding genes from human fetal hippocampus ESTs database","authors":"Keyue Ding, Xiaojing Sun, Min Zhou, Jing Cai, Tianjing Cai, Yan Zhang, Tongbin Zhu, Zhengguo Zhang, B. Qiang, Yan Shen","doi":"10.1002/NRC.10042","DOIUrl":"https://doi.org/10.1002/NRC.10042","url":null,"abstract":"We presented a procedure to identify novel protein-coding genes from human fetal hippocampus ESTs database generated in our previous study. The protocol is involved in searching the GenBank non-redundant (nr) protein database with ESTs coding regions query. We used ESTScan program to detect and reconstruct coding regions in the ESTs sequence data. With almost 10,000 raw ESTs analyzed, 4,061 coding regions were extracted. The corresponding amino acid sequences were then searched against the GenBank nr-protein databases; all the similarity hits were parsed in a homology analysis workbench. 22 ESTs were identified as the “seed” ESTs, which might be the fragment of the novel protein-coding genes. Indeed, further analysis of these ESTs in full-length cDNA cloning in silico, as well as the mapping information in UCSC and the added experimental proof, verified the effectiveness of the strategy. Taking advantage of rare ESTs resources, and the effective strategy, we would explore more novel genes in the human genome.\u0000 \u0000 \u0000 \u0000 [The ESTs sequence data described in this paper have been submitted to the GenBank data library (http://www.ncbi.nlm.nih.gov/dbEST) under accession nos. BM174886-958, BM259607-9; and the full length cDNA sequence can be obtained in http://www.chgb.org.cn/hippocampus.htm]","PeriodicalId":19198,"journal":{"name":"Neuroscience Research Communications","volume":"72 1","pages":"93-99"},"PeriodicalIF":0.0,"publicationDate":"2002-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"87270389","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Ş. Şahin, S. Sogut, H. Ozyurt, E. Uz, A. Ilhan, O. Akyol
Caffeic acid phenethyl ester exhibits antioxidant properties. This experimental study was designed to determine the effect of CAPE on nitric NO level and XO activity after reperfusion injury of spinal cord. New Zealand white rabbits were undergone aortic occlusion. CAPE, methylprednisolone or saline were injected intraperitoneally before surgical intervention. Animals were subjected to 21 min of crossclamp time. At the end of occlusion time, the clamps were removed and restoration of the blood flow was verified visually. Animals in sham group underwent a surgical procedure similar to the other groups but the aorta was not occluded. Spinal cord specimens were obtained to determine the tissue levels of NO and XO activity. Both XO activity and NO level in ischemia group were significantly higher than those of sham group (p = 0.0005 and 0.0003, respectively). MP and CAPE had no effect on XO activity after reperfusion. These two agents decreased NO levels nearly to that of sham group after reperfusion. There were no differences between MP and CAPE on reducing NO level. These results suggest that rabbits with ischemia-reperfusion injury in spinal cord have increased cord concentrations of nitrite and nitrate that are indicative of endogenous overproduction of NO. CAPE may be regarded as an agent that protects spinal cord from ischemia-reperfusion injury.
{"title":"Tissue xanthine oxidase activity and nitric oxide levels after spinal cord ischemia/reperfusion injury in rabbits: comparison of caffeic acid phenethyl ester (CAPE) and methylprednisolone","authors":"Ş. Şahin, S. Sogut, H. Ozyurt, E. Uz, A. Ilhan, O. Akyol","doi":"10.1002/NRC.10044","DOIUrl":"https://doi.org/10.1002/NRC.10044","url":null,"abstract":"Caffeic acid phenethyl ester exhibits antioxidant properties. This experimental study was designed to determine the effect of CAPE on nitric NO level and XO activity after reperfusion injury of spinal cord. New Zealand white rabbits were undergone aortic occlusion. CAPE, methylprednisolone or saline were injected intraperitoneally before surgical intervention. Animals were subjected to 21 min of crossclamp time. At the end of occlusion time, the clamps were removed and restoration of the blood flow was verified visually. Animals in sham group underwent a surgical procedure similar to the other groups but the aorta was not occluded. Spinal cord specimens were obtained to determine the tissue levels of NO and XO activity. \u0000 \u0000 \u0000 \u0000Both XO activity and NO level in ischemia group were significantly higher than those of sham group (p = 0.0005 and 0.0003, respectively). MP and CAPE had no effect on XO activity after reperfusion. These two agents decreased NO levels nearly to that of sham group after reperfusion. There were no differences between MP and CAPE on reducing NO level. These results suggest that rabbits with ischemia-reperfusion injury in spinal cord have increased cord concentrations of nitrite and nitrate that are indicative of endogenous overproduction of NO. CAPE may be regarded as an agent that protects spinal cord from ischemia-reperfusion injury.","PeriodicalId":19198,"journal":{"name":"Neuroscience Research Communications","volume":"42 1","pages":"111-121"},"PeriodicalIF":0.0,"publicationDate":"2002-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"85114301","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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