The mitogen-activated protein kinase (MAPK) family is involved in the regulation of cellular proliferation, differentiation and stress signals. In this study, we investigated the role of MAPK in response to H2O2, an oxidative stress, in neuronal cells. Activation of c-Jun-N-terminal kinase (JNK) was sustained, where as extracellular signal-regulated kinase (ERK) and p38 MAPK were transiently activated in response to H2O2 treatment. Inhibition of ERK and p38 resulted in higher activation of JNK in response to H2O2 treatment. The treatment with H2O2 led to apoptosis. The results implicate potential role of MAP kinases in neurodegenerative disorders mediated by oxidative stress.
丝裂原活化蛋白激酶(MAPK)家族参与细胞增殖、分化和应激信号的调控。在这项研究中，我们研究了MAPK在神经元细胞中响应H2O2(一种氧化应激)的作用。c- jun - n末端激酶(JNK)被持续激活，其中细胞外信号调节激酶(ERK)和p38 MAPK在H2O2处理下被短暂激活。抑制ERK和p38导致JNK在H2O2处理下的高活化。H2O2处理导致细胞凋亡。结果提示MAP激酶在氧化应激介导的神经退行性疾病中的潜在作用。
{"title":"Differential regulation of map kinase isoforms by H2O2 in neuronal cells","authors":"Amandeep Gargi, Naresh Kumar, C. Dey","doi":"10.1002/NRC.10077","DOIUrl":"https://doi.org/10.1002/NRC.10077","url":null,"abstract":"The mitogen-activated protein kinase (MAPK) family is involved in the regulation of cellular proliferation, differentiation and stress signals. In this study, we investigated the role of MAPK in response to H2O2, an oxidative stress, in neuronal cells. Activation of c-Jun-N-terminal kinase (JNK) was sustained, where as extracellular signal-regulated kinase (ERK) and p38 MAPK were transiently activated in response to H2O2 treatment. Inhibition of ERK and p38 resulted in higher activation of JNK in response to H2O2 treatment. The treatment with H2O2 led to apoptosis. The results implicate potential role of MAP kinases in neurodegenerative disorders mediated by oxidative stress.","PeriodicalId":19198,"journal":{"name":"Neuroscience Research Communications","volume":"103 1","pages":"17-29"},"PeriodicalIF":0.0,"publicationDate":"2003-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"86657731","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}
Neuroblastoma, the most common of all cancers found in children, may arise from a block of differentiation and a resultant continuation of the proliferative state. Neuroblastoma often spontaneously revert by undergoing partial differentiation and ultimate degeneration. A useful therapeutic approach for clinical neuroblastoma may encompass strategies to force neuroblastoma to differentiate. In ongoing studies on neuronal health, we have developed an anti-oxidant synergy formulation (“ASF”), comprised of α-tocopherol (vitamin E), sodium pyruvate and phosphatidyl choline, which lessens neurotoxicity and promotes axonal elaboration in cultured neurons. We demonstrate herein that ASF prevents proliferation and promotes differentiation of neuroblastoma in culture, even in the presence of serum, which normally induces rapid neuroblastoma proliferation in culture. These data leave open the possibility that ASF, with proper administration, may foster differentiation, and therefore ultimate degeneration, of neuroblastoma in situ, and may therefore represent a novel approach towards suppression of clinical neuroblastoma.
{"title":"An antitoxidant formulation that induces differentiation of neuroblastoma in culture","authors":"Amy L. Hancock, E. Nakuci, R. Nicolosi, T. Shea","doi":"10.1002/NRC.10082","DOIUrl":"https://doi.org/10.1002/NRC.10082","url":null,"abstract":"Neuroblastoma, the most common of all cancers found in children, may arise from a block of differentiation and a resultant continuation of the proliferative state. Neuroblastoma often spontaneously revert by undergoing partial differentiation and ultimate degeneration. A useful therapeutic approach for clinical neuroblastoma may encompass strategies to force neuroblastoma to differentiate. In ongoing studies on neuronal health, we have developed an anti-oxidant synergy formulation (“ASF”), comprised of α-tocopherol (vitamin E), sodium pyruvate and phosphatidyl choline, which lessens neurotoxicity and promotes axonal elaboration in cultured neurons. We demonstrate herein that ASF prevents proliferation and promotes differentiation of neuroblastoma in culture, even in the presence of serum, which normally induces rapid neuroblastoma proliferation in culture. These data leave open the possibility that ASF, with proper administration, may foster differentiation, and therefore ultimate degeneration, of neuroblastoma in situ, and may therefore represent a novel approach towards suppression of clinical neuroblastoma.","PeriodicalId":19198,"journal":{"name":"Neuroscience Research Communications","volume":"20 1","pages":"73-76"},"PeriodicalIF":0.0,"publicationDate":"2003-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"90296853","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}
F. Gokce, F. Bağırıcı, S. Kaplan, Ş. Demir, M. Ayyildiz, C. Marangoz
There are many studies on zinc as a possible cause of neuronal hyperactivity and cell death. The present study was designed to investigate the changes in total pyramidal cell number of rat hippocampus after intracortical zinc sulphate (ZnSO4, 200 μg/kg, i.c.) and a nitric oxide synthase (NOS) inhibitor aminoguanidine (AG) administration. Animals were divided into three groups as control, zinc and the treatment (zinc+AG) groups. Each group was divided into two subgroups, as 7-day group and 15-day group. Zinc sulphate was injected intracortically into 2 mm lateral of Bregma. The same volume of saline (2μl) was given to the rats belonging to the control groups. Rats in the third group were given ZnSO4 + AG in the same injection point. Animals in the third group only received 100 mg/kg AG intraperitoneally twice a day for periods of 7 or 15 days. Total pyramidal neuron number was estimated using the optical fractionator method. The total number of pyramidal cells found in the left hippocampus was 653,468 ± 3,452 and 601,860 ± 3,348 in the control groups; 257,968 ± 1,277 and 250,555 ± 1,443 in the zinc groups; 382,519 ± 1,973 and 365,880 ± 2,658 in the treatment groups in 7-day post treatment and 15-day post treatment rats, respectively. These results suggest that zinc has a neurotoxic effect on pyramidal neurons in rat hippocampus (p<0.05) and an inhibitor of nitric oxide synthase, AG, decreases cell loss (p<0.05). This shows that nitric oxide (NO) contributes to this type of neurotoxicity in the rat hippocampus and also suggests a possible therapeutic role for NOS inhibitor in neurodegenerative diseases.
{"title":"A NOS inhibitor aminoguanidine reduces zinc‐induced neuron loss in rat hippocampus","authors":"F. Gokce, F. Bağırıcı, S. Kaplan, Ş. Demir, M. Ayyildiz, C. Marangoz","doi":"10.1002/NRC.10080","DOIUrl":"https://doi.org/10.1002/NRC.10080","url":null,"abstract":"There are many studies on zinc as a possible cause of neuronal hyperactivity and cell death. The present study was designed to investigate the changes in total pyramidal cell number of rat hippocampus after intracortical zinc sulphate (ZnSO4, 200 μg/kg, i.c.) and a nitric oxide synthase (NOS) inhibitor aminoguanidine (AG) administration. Animals were divided into three groups as control, zinc and the treatment (zinc+AG) groups. Each group was divided into two subgroups, as 7-day group and 15-day group. Zinc sulphate was injected intracortically into 2 mm lateral of Bregma. The same volume of saline (2μl) was given to the rats belonging to the control groups. Rats in the third group were given ZnSO4 + AG in the same injection point. Animals in the third group only received 100 mg/kg AG intraperitoneally twice a day for periods of 7 or 15 days. Total pyramidal neuron number was estimated using the optical fractionator method. The total number of pyramidal cells found in the left hippocampus was 653,468 ± 3,452 and 601,860 ± 3,348 in the control groups; 257,968 ± 1,277 and 250,555 ± 1,443 in the zinc groups; 382,519 ± 1,973 and 365,880 ± 2,658 in the treatment groups in 7-day post treatment and 15-day post treatment rats, respectively. \u0000 \u0000 \u0000 \u0000These results suggest that zinc has a neurotoxic effect on pyramidal neurons in rat hippocampus (p<0.05) and an inhibitor of nitric oxide synthase, AG, decreases cell loss (p<0.05). This shows that nitric oxide (NO) contributes to this type of neurotoxicity in the rat hippocampus and also suggests a possible therapeutic role for NOS inhibitor in neurodegenerative diseases.","PeriodicalId":19198,"journal":{"name":"Neuroscience Research Communications","volume":"70 1","pages":"53-62"},"PeriodicalIF":0.0,"publicationDate":"2003-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"76446712","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 are interested in determining whether low maternal vitamin D-3 affects brain development in utero. Whilst the vitamin D receptor (VDR) has been identified in embryonic rat brains, the timing and magnitude of its expression across the brain remains unclear. In this study we have quantitated VDR expression during development as well correlated the timing of its appearance with two vital developmental events, apoptosis and mitosis. Brains from embryonic rats (embryonic days 15-23) were examined. We show that the well-described increase in apoptotic cells and decrease in mitotic cells during development correlates with the appearance of the VDR in brain tissue. Given that vitamin D-3 regulates mitosis and apoptosis in non-neuronal tissue we speculate that the timing of VDR expression in embryonic brain may directly or indirectly mediate features of neuronal apoptosis and mitosis.
{"title":"Vitamin D receptor expression in the embryonic rat brain","authors":"R. Burkert, J. Mcgrath, D. Eyles","doi":"10.1002/NRC.10081","DOIUrl":"https://doi.org/10.1002/NRC.10081","url":null,"abstract":"We are interested in determining whether low maternal vitamin D-3 affects brain development in utero. Whilst the vitamin D receptor (VDR) has been identified in embryonic rat brains, the timing and magnitude of its expression across the brain remains unclear. In this study we have quantitated VDR expression during development as well correlated the timing of its appearance with two vital developmental events, apoptosis and mitosis. Brains from embryonic rats (embryonic days 15-23) were examined. We show that the well-described increase in apoptotic cells and decrease in mitotic cells during development correlates with the appearance of the VDR in brain tissue. Given that vitamin D-3 regulates mitosis and apoptosis in non-neuronal tissue we speculate that the timing of VDR expression in embryonic brain may directly or indirectly mediate features of neuronal apoptosis and mitosis.","PeriodicalId":19198,"journal":{"name":"Neuroscience Research Communications","volume":"375 1","pages":"63-71"},"PeriodicalIF":0.0,"publicationDate":"2003-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"77390260","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}
Utilizing Fura 2-AM fluorescence photometry, intracellular calcium concentration ∥[Ca2+]i) was measured in wild type and dunce cleavage-arrested Drosophila neurons under resting condition and in response to KCl induced depolarization. Following KCl application, peak [Ca2+]i was greater in dunce (424 ± 29 nM) than in wild type neurons (246 ± 21 nM). Half decay time was shorter in dunce (65 ± 5 sec) than in wild type neurons (84 ± 6 sec). In cadmium-containing and in calcium-free external solutions, KCl application did not lead to any changes in [Ca2+]i in wild type and dunce neurons. Thus, the source of increase in [Ca2+]i seems to be Ca2+ influx from outside. Treatment with nifedipine and nimodipine did not affect [Ca2+]i increase in response to KCl application. This indicates that both wild type and dunce neuronal Ca2+ channels are not sensitive to these dihydropyridines. Pretreatment of wild type neurons with dibutyryl cAMP for 1 hour, prior to depolarization by KCl, resulted in peak [Ca2+]i of 369 ± 27 nM which is similar to untreated dunce neurons. The present results suggest that cAMP is implicated in modulating Ca2+ channels leading to enhanced Ca2+ influx in dunce neurons. Calcium extrusion and/or calcium buffering systems are possibly enhanced in the dunce mutant compared to the wild type. This disturbance in homeostatis of cytosolic calcium concentration in dunce neurons may be implicated in defective learning and memory.
{"title":"Differential effects of depolarization on intracellular calcium concentration in wild type and dunce Drosophila neurons","authors":"W. Alshuaib, M. Hasan, S. Cherian, M. Fahim","doi":"10.1002/NRC.10078","DOIUrl":"https://doi.org/10.1002/NRC.10078","url":null,"abstract":"Utilizing Fura 2-AM fluorescence photometry, intracellular calcium concentration ∥[Ca2+]i) was measured in wild type and dunce cleavage-arrested Drosophila neurons under resting condition and in response to KCl induced depolarization. Following KCl application, peak [Ca2+]i was greater in dunce (424 ± 29 nM) than in wild type neurons (246 ± 21 nM). Half decay time was shorter in dunce (65 ± 5 sec) than in wild type neurons (84 ± 6 sec). In cadmium-containing and in calcium-free external solutions, KCl application did not lead to any changes in [Ca2+]i in wild type and dunce neurons. Thus, the source of increase in [Ca2+]i seems to be Ca2+ influx from outside. Treatment with nifedipine and nimodipine did not affect [Ca2+]i increase in response to KCl application. This indicates that both wild type and dunce neuronal Ca2+ channels are not sensitive to these dihydropyridines. Pretreatment of wild type neurons with dibutyryl cAMP for 1 hour, prior to depolarization by KCl, resulted in peak [Ca2+]i of 369 ± 27 nM which is similar to untreated dunce neurons. The present results suggest that cAMP is implicated in modulating Ca2+ channels leading to enhanced Ca2+ influx in dunce neurons. Calcium extrusion and/or calcium buffering systems are possibly enhanced in the dunce mutant compared to the wild type. This disturbance in homeostatis of cytosolic calcium concentration in dunce neurons may be implicated in defective learning and memory.","PeriodicalId":19198,"journal":{"name":"Neuroscience Research Communications","volume":"57 1","pages":"31-43"},"PeriodicalIF":0.0,"publicationDate":"2003-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"85663681","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}
Aleksandar Kalauzi, M. Culic, L. Martac, G. Grbic, J. Saponjic, A. Jovanović, B. Janković, S. Spasic
The aim of this study was to reveal the nature and meaning of interspike background activity (RBA) recorded in Prukinje cell layer of rat cerebellum. We compared Fourier amtplitude spectra of recorded, extracted and averaged simple spike(s)—SS and complex spike(s)—CS with the mean amplitude spectrum of the remaining interspike RBA. A much greater similarity of spectral characteristics was noticed between SS and RBA, than between CS and RBA. Then, we simulated background activity (SBA), by superimposing averaged SS with randomized amplitudes and time delays. There was a significant correlation (p<0.005) between linearly transformed simulated and recorded amplitude spectra. Mean amplitude spectra of SBA were positively correlated with the number of superimposed SS. We propose to use this fact as a qualitative indication about the direction of change in the mean activity of surrounding neuronal population.
{"title":"New view on cerebellar cortical background activity in rat: simulation","authors":"Aleksandar Kalauzi, M. Culic, L. Martac, G. Grbic, J. Saponjic, A. Jovanović, B. Janković, S. Spasic","doi":"10.1002/NRC.10075","DOIUrl":"https://doi.org/10.1002/NRC.10075","url":null,"abstract":"The aim of this study was to reveal the nature and meaning of interspike background activity (RBA) recorded in Prukinje cell layer of rat cerebellum. We compared Fourier amtplitude spectra of recorded, extracted and averaged simple spike(s)—SS and complex spike(s)—CS with the mean amplitude spectrum of the remaining interspike RBA. A much greater similarity of spectral characteristics was noticed between SS and RBA, than between CS and RBA. Then, we simulated background activity (SBA), by superimposing averaged SS with randomized amplitudes and time delays. There was a significant correlation (p<0.005) between linearly transformed simulated and recorded amplitude spectra. Mean amplitude spectra of SBA were positively correlated with the number of superimposed SS. We propose to use this fact as a qualitative indication about the direction of change in the mean activity of surrounding neuronal population.","PeriodicalId":19198,"journal":{"name":"Neuroscience Research Communications","volume":"18 1","pages":"211-217"},"PeriodicalIF":0.0,"publicationDate":"2003-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"78611281","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 rutabaga mutation which has a low intracellular cyclic adenosine monophosphate (cAMP) concentration is defective in short-term memory. The aim of this study was to compare modulation effects of dopamine on the delayed-rectifier potassium current (IKDR) in rutabaga and wild-type Drosophila neurons. The conventional whole-cell patch-clamp technique was applied to cultured Drosophila neurons derived from embryonic neuroblasts. IKDR was measured from cultured (2 days) wild-type and rutabaga neurons. IKDR was smaller in rutabaga neurons (373 ± 38 pA) than in wild-type neurons (519 ± 40 pA) but there was no difference in IKDR activation in wild-type inactivation between the two genotypes. We examined the effects of dopamine on IKDR in wild-type and rutabaga neurons. IKDR was measured from neurons before and after addition of dopamine to the external solution. Dopamine application reduced IKDR in wild-type neurons but did not significantly affect IKDR in rutabaga neurons (single-cell studies). In the presence of dopamine there was no difference in IKDR between wild-type (344 ± 29 pA) and rutabaga (338 ± 27pA) neurons (population studies). These results indicate that dopamine differentially affects the delayed-rectifier channel in wild-type and rutabaga neurons. This can alter neuronal excitability in rutabaga and may affect the processing of neural signals necessary for learning and memory.
{"title":"Differential effects of dopamine on a potassium current in cultured rutabaga and wild-type Drosophila cells","authors":"W. Alshuaib, M. V. Mathew, M. Hasan, M. Fahim","doi":"10.1002/NRC.10072","DOIUrl":"https://doi.org/10.1002/NRC.10072","url":null,"abstract":"The rutabaga mutation which has a low intracellular cyclic adenosine monophosphate (cAMP) concentration is defective in short-term memory. The aim of this study was to compare modulation effects of dopamine on the delayed-rectifier potassium current (IKDR) in rutabaga and wild-type Drosophila neurons. The conventional whole-cell patch-clamp technique was applied to cultured Drosophila neurons derived from embryonic neuroblasts. IKDR was measured from cultured (2 days) wild-type and rutabaga neurons. IKDR was smaller in rutabaga neurons (373 ± 38 pA) than in wild-type neurons (519 ± 40 pA) but there was no difference in IKDR activation in wild-type inactivation between the two genotypes. We examined the effects of dopamine on IKDR in wild-type and rutabaga neurons. IKDR was measured from neurons before and after addition of dopamine to the external solution. Dopamine application reduced IKDR in wild-type neurons but did not significantly affect IKDR in rutabaga neurons (single-cell studies). In the presence of dopamine there was no difference in IKDR between wild-type (344 ± 29 pA) and rutabaga (338 ± 27pA) neurons (population studies). These results indicate that dopamine differentially affects the delayed-rectifier channel in wild-type and rutabaga neurons. This can alter neuronal excitability in rutabaga and may affect the processing of neural signals necessary for learning and memory.","PeriodicalId":19198,"journal":{"name":"Neuroscience Research Communications","volume":"23 1","pages":"175-187"},"PeriodicalIF":0.0,"publicationDate":"2003-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"85204678","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}
Despite strong homology between subunits of AMPA-type glutamate receptors, heteromeric assemblies in different brain regions vary in subunit composition and functional properties. We have previously shown that charge substitution at K445 decreases the apparent potency of AMPA for GluR-A receptors, although an analogous mutation is a low conductance B subunit of AB heteromers did not diminish AMPA potency. To examine the subunit selectivity of K445, we now measure the apparent potency of AMPA and glutamate at recombinant homomeric receptors containing the high-conductance, unedited (586Q) GluR-B subunit (GluR-B(Q)) using two-electrode voltage-clamp. We find the decrease in apparent potency of AMPA is recapitulated for homomeric GluR-B(Q)K449E receptors, and is rescued by coexpression with wild-type GluR-A. These data are consistent with the hypothesis that AMPAR subunit composition is critical to agonist-dependent receptor activation, and suggest that GluR-A plays a dominant role in mediating receptor activation by AMPA.
{"title":"Lysine 445 is a molecular indicator of subunit‐specific AMPA receptor binding domains","authors":"J. S. S. Sikes, T. Verdoorn","doi":"10.1002/NRC.10069","DOIUrl":"https://doi.org/10.1002/NRC.10069","url":null,"abstract":"Despite strong homology between subunits of AMPA-type glutamate receptors, heteromeric assemblies in different brain regions vary in subunit composition and functional properties. We have previously shown that charge substitution at K445 decreases the apparent potency of AMPA for GluR-A receptors, although an analogous mutation is a low conductance B subunit of AB heteromers did not diminish AMPA potency. To examine the subunit selectivity of K445, we now measure the apparent potency of AMPA and glutamate at recombinant homomeric receptors containing the high-conductance, unedited (586Q) GluR-B subunit (GluR-B(Q)) using two-electrode voltage-clamp. We find the decrease in apparent potency of AMPA is recapitulated for homomeric GluR-B(Q)K449E receptors, and is rescued by coexpression with wild-type GluR-A. These data are consistent with the hypothesis that AMPAR subunit composition is critical to agonist-dependent receptor activation, and suggest that GluR-A plays a dominant role in mediating receptor activation by AMPA.","PeriodicalId":19198,"journal":{"name":"Neuroscience Research Communications","volume":"15 1","pages":"143-150"},"PeriodicalIF":0.0,"publicationDate":"2003-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"87209928","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}
There have been numerous studies of neuronal hyperactivity and oxidative stress induced by iron. Moreover, it has been found that iron levels in the brain are markedly increased in some neurodegenerative diseases such as Alzheimer's disease (AD) and Parkinson's disease (PD). We attempted to identify the toxic effect of iron on the hippocampus, a region of the brain known to be involved in learning and memory processes and which lends itself to stereological analysis. Rats were given iron chloride (FeCl35H2O), 200 mM in 2.5 μl) intracortically and were killed 10 days later. The total number of neurons in the hippocampus of control and iron-treated rats was counted with an optical fractionator. Iron administration caused a significant decrease in the total number of pyramidal neurons in the left (31.6% decrease) and right (32.2% decrease) hippocampi (p<0.001). The findings suggest that excess iron contributes to pyramidal cell death in the rat hippocampus.
目前已有大量关于铁诱导的神经元过度活跃和氧化应激的研究。此外，研究发现，在一些神经退行性疾病，如阿尔茨海默病(AD)和帕金森病(PD)中，大脑中的铁水平显著升高。我们试图确定铁对海马体的毒性作用，海马体是大脑中一个已知参与学习和记忆过程的区域，适合进行立体学分析。大鼠皮质灌胃氯化铁(FeCl35H2O) 200 mM (2.5 μl)， 10 d后处死。用光学分数仪对对照组和铁处理大鼠海马神经元总数进行计数。铁处理导致大鼠左、右海马锥体神经元总数显著减少(分别减少31.6%和32.2%)(p<0.001)。研究结果表明，过量的铁有助于大鼠海马锥体细胞死亡。
{"title":"The neurotoxic effect of iron on pyramidal cell number in rat hippocampus: a stereological study","authors":"M. O. Bostanci, F. Bağırıcı, A. Korkmaz","doi":"10.1002/NRC.10070","DOIUrl":"https://doi.org/10.1002/NRC.10070","url":null,"abstract":"There have been numerous studies of neuronal hyperactivity and oxidative stress induced by iron. Moreover, it has been found that iron levels in the brain are markedly increased in some neurodegenerative diseases such as Alzheimer's disease (AD) and Parkinson's disease (PD). We attempted to identify the toxic effect of iron on the hippocampus, a region of the brain known to be involved in learning and memory processes and which lends itself to stereological analysis. Rats were given iron chloride (FeCl35H2O), 200 mM in 2.5 μl) intracortically and were killed 10 days later. The total number of neurons in the hippocampus of control and iron-treated rats was counted with an optical fractionator. Iron administration caused a significant decrease in the total number of pyramidal neurons in the left (31.6% decrease) and right (32.2% decrease) hippocampi (p<0.001). The findings suggest that excess iron contributes to pyramidal cell death in the rat hippocampus.","PeriodicalId":19198,"journal":{"name":"Neuroscience Research Communications","volume":"38 1","pages":"151-159"},"PeriodicalIF":0.0,"publicationDate":"2003-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"73819321","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}
Optic flow analysis has been extensively investigated in several extrastriate visual areas of the primate, but it remains unclear whether and how the striate cortex is involved in the processing. In the present study 156 striate neurons in anaesthetized cats were tested with simulated optic flow patterns. More than 80% of the cells responded to the stimuli, about 30% significantly preferred translation to radiation and rotation, but few, if any, displayed clear preference for radial or circular motion. Most responsive neurons had fairly good direction sensitivity for their optimal stimuli. Generally, the differences between simple and complex cells were small and insignificant. Although translation obviously prevailed over radiation and rotation in driving more cells and eliciting stronger responses, the responsivity to complex flow fields was not predictable with the direction preference to planar motion. These results suggest that the striate contribution to optic flow analysis may go beyond the direction selectivity to local translation and there might be some kind of specific mechanism to complex motion features.
{"title":"Response properties of cat striate neurons to simulated optic flow stimuli","authors":"Baowang Li, Bing-chuan Li, Yao Chen, Y. Diao","doi":"10.1002/NRC.10074","DOIUrl":"https://doi.org/10.1002/NRC.10074","url":null,"abstract":"Optic flow analysis has been extensively investigated in several extrastriate visual areas of the primate, but it remains unclear whether and how the striate cortex is involved in the processing. In the present study 156 striate neurons in anaesthetized cats were tested with simulated optic flow patterns. More than 80% of the cells responded to the stimuli, about 30% significantly preferred translation to radiation and rotation, but few, if any, displayed clear preference for radial or circular motion. Most responsive neurons had fairly good direction sensitivity for their optimal stimuli. Generally, the differences between simple and complex cells were small and insignificant. Although translation obviously prevailed over radiation and rotation in driving more cells and eliciting stronger responses, the responsivity to complex flow fields was not predictable with the direction preference to planar motion. These results suggest that the striate contribution to optic flow analysis may go beyond the direction selectivity to local translation and there might be some kind of specific mechanism to complex motion features.","PeriodicalId":19198,"journal":{"name":"Neuroscience Research Communications","volume":"1 1","pages":"197-210"},"PeriodicalIF":0.0,"publicationDate":"2003-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"83003109","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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