Seung-Won Park, Young Baeg Kim, B. Min, Sung-nam Hwang, J. Kwon, J. Suk
We investigated the spatial characteristics of apoptotic genes expression and CBF at the ischemic penumbra. A delayed focal cerebral infarction was created in twelve adult Sprague-Dawley rats. Immunohistochemical staining of bcl-2 and p53 proteins and TUNEL staining for apoptosis were performed. The peri-infarct area was divided into six sectors by distance from the infarction border. Local CBF was measured at 2 mm distal to the presumed MCA occlusion site preoperatively, and at 2 mm and 8 mm distal to the MCA occlusion site intraoperatively. TUNEL-positive, bcl-2 or p53 positive cells were concentrated as it went closer to the infarction core and reduced peripherally, which was inversely proportional to the local CBF. The area encompassed by the border of the p53 area was 3.3 ± 0.2 times of the infarction core. The p53 area seems to overlap the ischemic penumbra, and may deserve to be a molecular penumbra.
{"title":"p53, bcl-2 Protein expression and the level of cerebral blood flow at the ischemic penumbra in rats","authors":"Seung-Won Park, Young Baeg Kim, B. Min, Sung-nam Hwang, J. Kwon, J. Suk","doi":"10.1002/NRC.10098","DOIUrl":"https://doi.org/10.1002/NRC.10098","url":null,"abstract":"We investigated the spatial characteristics of apoptotic genes expression and CBF at the ischemic penumbra. A delayed focal cerebral infarction was created in twelve adult Sprague-Dawley rats. Immunohistochemical staining of bcl-2 and p53 proteins and TUNEL staining for apoptosis were performed. The peri-infarct area was divided into six sectors by distance from the infarction border. Local CBF was measured at 2 mm distal to the presumed MCA occlusion site preoperatively, and at 2 mm and 8 mm distal to the MCA occlusion site intraoperatively. TUNEL-positive, bcl-2 or p53 positive cells were concentrated as it went closer to the infarction core and reduced peripherally, which was inversely proportional to the local CBF. The area encompassed by the border of the p53 area was 3.3 ± 0.2 times of the infarction core. The p53 area seems to overlap the ischemic penumbra, and may deserve to be a molecular penumbra.","PeriodicalId":19198,"journal":{"name":"Neuroscience Research Communications","volume":"40 1","pages":"218-226"},"PeriodicalIF":0.0,"publicationDate":"2003-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"85580387","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}
Mustafa Sarsimaz, A. Songur, İ. Kuş, B. Ozyurt, M. Gulec, S. Sogut, A. Ilhan, O. Akyol
Omega-3 essential fatty acids (ω-3 EFA) contains eicosapentaenoic acid and docosahexaenoic acid (DHA). DHA is one of the building structures of membrane phospholipids of brain and necessary for continuity of neuronal functions. ω-3 EFA has been suggested to be protective against neuropsychiatric disorders including schizophrenia. This study proposed to assess the changes in superoxide dismutase (SOD), xanthine oxidase (XO), malondialdehyde (MDA), and nitric oxide (NO) in the hippocampus of rats fed with ω-3 diet (0.4 g/kg/day) for 30 days. Eight control rats and nine rats fed with ω-3 EFA were decapitated under ether anesthesia, and hippocampus was removed immediately. Rats treated with ω-3 EFA had significatly lower XO activity (p<0.002) and NO level (p<0.0001) whereas higher SOD activity (p<0.002) and MDA levels (p<0.019) than the control rats. These results suggest that the dietary ω-3 EFA may act on the oxidant/antioxidant parameters in hippocampus. On the other hand, although the mechanism is not clear, ω-3 EFA may enhance one of the most important antioxidant enzymes, SOD. Further studies are needed to clarify the molecular mechanism involved and the therapeutic implication of ω-3 EFA in animal psychosis models and clinical studies.
{"title":"The regulatory role of dietary ω-3 essential fatty acids on oxidant/antioxidant balance in rat hippocampus","authors":"Mustafa Sarsimaz, A. Songur, İ. Kuş, B. Ozyurt, M. Gulec, S. Sogut, A. Ilhan, O. Akyol","doi":"10.1002/NRC.10087","DOIUrl":"https://doi.org/10.1002/NRC.10087","url":null,"abstract":"Omega-3 essential fatty acids (ω-3 EFA) contains eicosapentaenoic acid and docosahexaenoic acid (DHA). DHA is one of the building structures of membrane phospholipids of brain and necessary for continuity of neuronal functions. ω-3 EFA has been suggested to be protective against neuropsychiatric disorders including schizophrenia. This study proposed to assess the changes in superoxide dismutase (SOD), xanthine oxidase (XO), malondialdehyde (MDA), and nitric oxide (NO) in the hippocampus of rats fed with ω-3 diet (0.4 g/kg/day) for 30 days. Eight control rats and nine rats fed with ω-3 EFA were decapitated under ether anesthesia, and hippocampus was removed immediately. \u0000 \u0000 \u0000 \u0000Rats treated with ω-3 EFA had significatly lower XO activity (p<0.002) and NO level (p<0.0001) whereas higher SOD activity (p<0.002) and MDA levels (p<0.019) than the control rats. These results suggest that the dietary ω-3 EFA may act on the oxidant/antioxidant parameters in hippocampus. On the other hand, although the mechanism is not clear, ω-3 EFA may enhance one of the most important antioxidant enzymes, SOD. Further studies are needed to clarify the molecular mechanism involved and the therapeutic implication of ω-3 EFA in animal psychosis models and clinical studies.","PeriodicalId":19198,"journal":{"name":"Neuroscience Research Communications","volume":"1 1","pages":"114-123"},"PeriodicalIF":0.0,"publicationDate":"2003-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"83405267","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}
Xin-yu Yu, Yongqui Wang Ceballos, Hong Zhao, Zhongqui Xu
Glutamate-induced neuronal apoptosis plays an important role in neurodegenerative disorders. In the process of screening for naturally occurring substances with neuroprotective effects against glutamate exitotoxicity, we have discovered that the extract from Alpinia oxyphylla, a traditional Chinese medicinal herb, exhibited significant neuroprotective activity against glutamate exitotoxicity in cultured cortical neurons. The present study was designed to investigate the protective effect of Alpinia oxyphylla extract against glutamate-induced neuronal apoptosis in primary cultured mouse cortical neurons. After exposure of the neurons to glutamate (30 μM), apoptotic cell death was observed as evidenced by alteration of neuronal morphology, DNA fragmentation on agarose gel and flow cytometric analysis. Co-treatment of the neurons with Alpinia oxyphylla extract (80–240 μg/ml) in the presence of glutamate significantly elevated the cell viability, reduced the number of apoptotic cells and decreased the intensity of glutamate-induced DNA fragmentation. The results suggest the neuroprotective potential of Alpinia oxyphylla against glutamate-induced neuronal apoptosis.
{"title":"Neuroprotective effect of Alpinia oxyphylla extract against glutamate‐induced apoptosis in cultured mouse cortical neurons","authors":"Xin-yu Yu, Yongqui Wang Ceballos, Hong Zhao, Zhongqui Xu","doi":"10.1002/NRC.10086","DOIUrl":"https://doi.org/10.1002/NRC.10086","url":null,"abstract":"Glutamate-induced neuronal apoptosis plays an important role in neurodegenerative disorders. In the process of screening for naturally occurring substances with neuroprotective effects against glutamate exitotoxicity, we have discovered that the extract from Alpinia oxyphylla, a traditional Chinese medicinal herb, exhibited significant neuroprotective activity against glutamate exitotoxicity in cultured cortical neurons. The present study was designed to investigate the protective effect of Alpinia oxyphylla extract against glutamate-induced neuronal apoptosis in primary cultured mouse cortical neurons. After exposure of the neurons to glutamate (30 μM), apoptotic cell death was observed as evidenced by alteration of neuronal morphology, DNA fragmentation on agarose gel and flow cytometric analysis. Co-treatment of the neurons with Alpinia oxyphylla extract (80–240 μg/ml) in the presence of glutamate significantly elevated the cell viability, reduced the number of apoptotic cells and decreased the intensity of glutamate-induced DNA fragmentation. The results suggest the neuroprotective potential of Alpinia oxyphylla against glutamate-induced neuronal apoptosis.","PeriodicalId":19198,"journal":{"name":"Neuroscience Research Communications","volume":"78 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2003-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"87100398","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}
M. Jang, M. Shin, Hong Kim, Ee-Hwa Kim, Chang-Ju Kim
Serotonin (5-hydroxytryptamine, 5-HT) has been implicated in the pathophysiology of many neuropsychiatric disorders, and alcohol is reported to influence serotonergic neuronal activity in the dorsal raphe. In the present study, the effects of ethanol on the synthesis of 5-HT and the expression of tryptophan hydroxylase (TPH), the rate-limiting enzyme of 5-HT synthesis, in the dorsal and median raphe of rats were investigated, using immunohistochemial methods. Results showed that the density of 5-HT-positive and TPH-positive cells was reduced by ethanol treatment in a time-dependent manner. Based on these results, it is suggested that the pathogenesis of ethanol-induced neuropsychological disorders involves ethanol-induced suppression of 5-HT synthesis and TPH expression in the raphe region.
{"title":"Time dependence of the effect of ethanol on serotonin synthesis and tryptophan hydroxylase expression in the dorsal and median raphe of young rats","authors":"M. Jang, M. Shin, Hong Kim, Ee-Hwa Kim, Chang-Ju Kim","doi":"10.1002/NRC.10085","DOIUrl":"https://doi.org/10.1002/NRC.10085","url":null,"abstract":"Serotonin (5-hydroxytryptamine, 5-HT) has been implicated in the pathophysiology of many neuropsychiatric disorders, and alcohol is reported to influence serotonergic neuronal activity in the dorsal raphe. In the present study, the effects of ethanol on the synthesis of 5-HT and the expression of tryptophan hydroxylase (TPH), the rate-limiting enzyme of 5-HT synthesis, in the dorsal and median raphe of rats were investigated, using immunohistochemial methods. Results showed that the density of 5-HT-positive and TPH-positive cells was reduced by ethanol treatment in a time-dependent manner. Based on these results, it is suggested that the pathogenesis of ethanol-induced neuropsychological disorders involves ethanol-induced suppression of 5-HT synthesis and TPH expression in the raphe region.","PeriodicalId":19198,"journal":{"name":"Neuroscience Research Communications","volume":"110 1","pages":"99-104"},"PeriodicalIF":0.0,"publicationDate":"2003-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"79509760","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}
Cbl regulates receptor tyrosine kinase activity by promoting the endocytosis of receptors from the plasma membrane. The mechanism of this effect is unclear, but recent evidence suggests that Cbl mediates ubiquitin-dependent sorting of receptors following recruitment to phosphotyrosine motifs in the activated receptor. Moreover, recent findings support a role for Cbl in the clathrin-mediated endocytosis of receptor tyrosine kinases. We provide evidence that Cbl is found in complex with clathrin and is localized to clathrin-coated vesicles following NGF stimulation of TrkA. We also show that overexpression of Cbl enhances clathrin-mediated endocytosis of 125I-NFG, and that this increased internalization is correlated with a substantial acceleration of neurite outgrowth in response to NGF. Our data suggest that Cbl may participate in the formation of a multi-protein complex involved in the clathrin-mediated endocytosis of receptor tyrosine kinases, and that Cbl may function as a positive regulator of such kinases in specific cellular contexts.
{"title":"A Cbl:clathrin complex involved in NGF signaling for neurite outgrowth","authors":"C. Howe","doi":"10.1002/NRC.10084","DOIUrl":"https://doi.org/10.1002/NRC.10084","url":null,"abstract":"Cbl regulates receptor tyrosine kinase activity by promoting the endocytosis of receptors from the plasma membrane. The mechanism of this effect is unclear, but recent evidence suggests that Cbl mediates ubiquitin-dependent sorting of receptors following recruitment to phosphotyrosine motifs in the activated receptor. Moreover, recent findings support a role for Cbl in the clathrin-mediated endocytosis of receptor tyrosine kinases. We provide evidence that Cbl is found in complex with clathrin and is localized to clathrin-coated vesicles following NGF stimulation of TrkA. We also show that overexpression of Cbl enhances clathrin-mediated endocytosis of 125I-NFG, and that this increased internalization is correlated with a substantial acceleration of neurite outgrowth in response to NGF. Our data suggest that Cbl may participate in the formation of a multi-protein complex involved in the clathrin-mediated endocytosis of receptor tyrosine kinases, and that Cbl may function as a positive regulator of such kinases in specific cellular contexts.","PeriodicalId":19198,"journal":{"name":"Neuroscience Research Communications","volume":"12 1","pages":"86-98"},"PeriodicalIF":0.0,"publicationDate":"2003-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"73112752","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}
Oxygen-derived free radicals have been implicated in the pathogenesis of doxorubicin-induced toxicities. The aim of this study was to investigate the effects of caffeic acid phenethyl ester (CAPE), an antioxidant agent, on doxorubicin-induced neuronal oxidative injury in rats. The rats were treated with CAPE (10μmol/kg/day i.p.) or saline starting 2 days before a single dose of doxorubicin (20 mg/kg i.p.) or saline. Ten days after the first experiments, the brain was excised to analyze the activities of antioxidant enzymes and levels of malondialdehyde (MDA) and nitric oxide (NO). Doxorubicin alone resulted in higher MDA level in brain tissue than the other groups. The activity of catalase was higher in doxorubicin plus CAPE group than doxorubicin group. There were no significant differences in NO level, glutathione peroxidase (GSH-Px) and superoxide dismutase activities between the groups. There were negative correlations between GSG-Px activity and MDA level in both doxorubicin and doxorubicin plus CAPE groups. It can be concluded that doxorubicin induced oxidant injury can be prevented by CAPE treatment through its antioxidant properties in rat brain.
{"title":"Effects of caffeic acid phenethyl ester against doxorubicin‐induced neuronal oxidant injury","authors":"E. Fadillioglu, H. Erdoğan, M. Iraz, M. Yağmurca","doi":"10.1002/NRC.10089","DOIUrl":"https://doi.org/10.1002/NRC.10089","url":null,"abstract":"Oxygen-derived free radicals have been implicated in the pathogenesis of doxorubicin-induced toxicities. The aim of this study was to investigate the effects of caffeic acid phenethyl ester (CAPE), an antioxidant agent, on doxorubicin-induced neuronal oxidative injury in rats. The rats were treated with CAPE (10μmol/kg/day i.p.) or saline starting 2 days before a single dose of doxorubicin (20 mg/kg i.p.) or saline. Ten days after the first experiments, the brain was excised to analyze the activities of antioxidant enzymes and levels of malondialdehyde (MDA) and nitric oxide (NO). Doxorubicin alone resulted in higher MDA level in brain tissue than the other groups. The activity of catalase was higher in doxorubicin plus CAPE group than doxorubicin group. There were no significant differences in NO level, glutathione peroxidase (GSH-Px) and superoxide dismutase activities between the groups. There were negative correlations between GSG-Px activity and MDA level in both doxorubicin and doxorubicin plus CAPE groups. It can be concluded that doxorubicin induced oxidant injury can be prevented by CAPE treatment through its antioxidant properties in rat brain.","PeriodicalId":19198,"journal":{"name":"Neuroscience Research Communications","volume":"36 1","pages":"132-138"},"PeriodicalIF":0.0,"publicationDate":"2003-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"74669657","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}
We have investigated the effects of verapamil, which blocks L-type calcium channels on spinal monosynaptic reflexes in spinalized cats. Adult cats (n=10) weighing 1.5–3 kg were anaesthetized with ketamine (50 mg/kg, IM) and the ventral and dorsal roots of segment L5-S2 were isolated after laminectomy. The lateral and medial gastrocnemius nerves were placed on an Ag-AgCl wire electrode for stimulation through an isolation unit. The reflex potentials were recorded from the ipsilateral L7 ventral root. The intraperitoneal administration of verapamil significantly decreased the amplitude of the reflex response (P<0.05). Our results suggest that L-type calcium channels in the spinal cord may play an important role in regulating the reflex response.
{"title":"The role of L‐type calcium channels in spinal reflex responses in cats","authors":"N. Tasci, O. Genć, F. Bağırıcı","doi":"10.1002/NRC.10088","DOIUrl":"https://doi.org/10.1002/NRC.10088","url":null,"abstract":"We have investigated the effects of verapamil, which blocks L-type calcium channels on spinal monosynaptic reflexes in spinalized cats. Adult cats (n=10) weighing 1.5–3 kg were anaesthetized with ketamine (50 mg/kg, IM) and the ventral and dorsal roots of segment L5-S2 were isolated after laminectomy. The lateral and medial gastrocnemius nerves were placed on an Ag-AgCl wire electrode for stimulation through an isolation unit. The reflex potentials were recorded from the ipsilateral L7 ventral root. The intraperitoneal administration of verapamil significantly decreased the amplitude of the reflex response (P<0.05). Our results suggest that L-type calcium channels in the spinal cord may play an important role in regulating the reflex response.","PeriodicalId":19198,"journal":{"name":"Neuroscience Research Communications","volume":"1 1","pages":"124-131"},"PeriodicalIF":0.0,"publicationDate":"2003-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"75351644","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}
The mammalian and avian striatum are homologous structures, while the mammalian prefrontal cortex (PFC) and the avian neostriatum caudolaterale (NCL) represent functionally equivalent, possibly homoplastic structures. We used brain microdialysis to study basal levels and release mechanisms of dopamine (DA) and serotonin (5-HT) in the pigeons' forebrain to be able to compare the biochemical characteristics between these structures and different species. Basal DA levels in the pigeons' NCL were different from those in the rats' PFC, but were similar in the striatum. This was converse for 5-HT. As in mammals, perfusion with artificial cerebrospinal fluid (aCSF) with elevated potassium significantly increased DA levels, whereas calcium-free aCSF decreased the DA efflux. In summary, the avian and mammalian forebrains show a complex pattern of neurochemical similarities and differences. These data suggest that absolute and relative concentrations of modulatory systems may change considerably over evolutionary time, while basic biochemical mechanismsm stay unaltered.
{"title":"Comparative neurochemistry of the avian forebrain and striatum: a microdialysis study","authors":"Dilek Karakuyu, B. Diekamp, O. Güntürkün","doi":"10.1002/NRC.10090","DOIUrl":"https://doi.org/10.1002/NRC.10090","url":null,"abstract":"The mammalian and avian striatum are homologous structures, while the mammalian prefrontal cortex (PFC) and the avian neostriatum caudolaterale (NCL) represent functionally equivalent, possibly homoplastic structures. We used brain microdialysis to study basal levels and release mechanisms of dopamine (DA) and serotonin (5-HT) in the pigeons' forebrain to be able to compare the biochemical characteristics between these structures and different species. Basal DA levels in the pigeons' NCL were different from those in the rats' PFC, but were similar in the striatum. This was converse for 5-HT. As in mammals, perfusion with artificial cerebrospinal fluid (aCSF) with elevated potassium significantly increased DA levels, whereas calcium-free aCSF decreased the DA efflux. In summary, the avian and mammalian forebrains show a complex pattern of neurochemical similarities and differences. These data suggest that absolute and relative concentrations of modulatory systems may change considerably over evolutionary time, while basic biochemical mechanismsm stay unaltered.","PeriodicalId":19198,"journal":{"name":"Neuroscience Research Communications","volume":"123 1","pages":"139-146"},"PeriodicalIF":0.0,"publicationDate":"2003-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"76169729","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}
H. Salgado-Ceballos, I. Grijalva, G. Guízar-Sahagún, A. Espitia, Angelina Martínez, A. Feria-Velasco
Traumatic spinal cord injury (TSCI) produces paralysis by destruction of axons and demyelination of surviving fibers. Using methylprednisolone (MP) as neuroprotector and a predegenerated peripheral nerve (PPN) graft as regenerative strategy, 83 rats with TSCI were divided into non-grafted, fresh peripheral nerve (FPN) and PPN grafted groups with and without MP administration. Myelination index (MI), number of axons, myelinated fibers, and axon collaterals were assessed 21 h, 7 days, 2, and 4 months after TSCI. Animals with PPN grafts showed more axons and myelinated fibers than animals with FPN grafts, while the latter showed the highest number of axon collaterals. When MP was used, collateral emission was decreased in all treated groups. However, PPN graft plus MP group had the best MI and highest number of axons and myelinated fibers. Combination of one neuroprotective with a regenerative strategy is a good therapeutic option, although new combinations should be further explored.
{"title":"Predegenerated peripheral nerve graft with and without methylprednisolone administration after traumatic spinal cord injury in adult rats","authors":"H. Salgado-Ceballos, I. Grijalva, G. Guízar-Sahagún, A. Espitia, Angelina Martínez, A. Feria-Velasco","doi":"10.1002/NRC.10083","DOIUrl":"https://doi.org/10.1002/NRC.10083","url":null,"abstract":"Traumatic spinal cord injury (TSCI) produces paralysis by destruction of axons and demyelination of surviving fibers. Using methylprednisolone (MP) as neuroprotector and a predegenerated peripheral nerve (PPN) graft as regenerative strategy, 83 rats with TSCI were divided into non-grafted, fresh peripheral nerve (FPN) and PPN grafted groups with and without MP administration. Myelination index (MI), number of axons, myelinated fibers, and axon collaterals were assessed 21 h, 7 days, 2, and 4 months after TSCI. Animals with PPN grafts showed more axons and myelinated fibers than animals with FPN grafts, while the latter showed the highest number of axon collaterals. When MP was used, collateral emission was decreased in all treated groups. However, PPN graft plus MP group had the best MI and highest number of axons and myelinated fibers. Combination of one neuroprotective with a regenerative strategy is a good therapeutic option, although new combinations should be further explored.","PeriodicalId":19198,"journal":{"name":"Neuroscience Research Communications","volume":"46 1","pages":"77-85"},"PeriodicalIF":0.0,"publicationDate":"2003-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"82667003","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}
Haiwei Xu, Xiaotang Fan, Enquan Gao, Xuan Wu, Juan Cao, Haidi Li
SIJMMARY Melatonin deficiency in cerebrospinal fluid has been postulated to be critical for the development of Alzheimer Disease (AD). As a potent free radical scavengers and antioxidant, melatonin has been proposed to delay or inhibit progression of neurodegeneration in AD. Since the effect of melatonin on AP peptide toxicity in the rat oxidative stress model of AD is not fully understood, we observed the effect of melatonin on AP protein and APP mRNA in the hippocampus and frontal cortex of AD rats model established by Bennett and found melatonin inhibited the AP and APP mRNA . The effect of melatonin could be partly attenuated by pretreatment with the GABA antagonist bicuculline. The results suggest melatonin reduced the AP production probably by inhibiting overexpression of APP in the CNS of AD model rats. Maybe these effects of melatonin were influenced by GABA.
{"title":"Effect of melatonin on β-amyloid peptide overexpression and memory impairment in a rat AD-model and the influence of bicuculline","authors":"Haiwei Xu, Xiaotang Fan, Enquan Gao, Xuan Wu, Juan Cao, Haidi Li","doi":"10.1002/NRC.10079","DOIUrl":"https://doi.org/10.1002/NRC.10079","url":null,"abstract":"SIJMMARY Melatonin deficiency in cerebrospinal fluid has been postulated to be critical for the development of Alzheimer Disease (AD). As a potent free radical scavengers and antioxidant, melatonin has been proposed to delay or inhibit progression of neurodegeneration in AD. Since the effect of melatonin on AP peptide toxicity in the rat oxidative stress model of AD is not fully understood, we observed the effect of melatonin on AP protein and APP mRNA in the hippocampus and frontal cortex of AD rats model established by Bennett and found melatonin inhibited the AP and APP mRNA . The effect of melatonin could be partly attenuated by pretreatment with the GABA antagonist bicuculline. The results suggest melatonin reduced the AP production probably by inhibiting overexpression of APP in the CNS of AD model rats. Maybe these effects of melatonin were influenced by GABA.","PeriodicalId":19198,"journal":{"name":"Neuroscience Research Communications","volume":"29 1","pages":"44-52"},"PeriodicalIF":0.0,"publicationDate":"2003-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"81097990","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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