The laminar distribution of the neurofilament inclusions (NI) and swollen achromatic neurons (SN) was studied in gyri of the temporal cortex in four patients with neurofilament inclusion disease (NID). In 84% of gyri analysed, the density of the NI was maximal in the lower cortical laminae. The distribution of the SN was more variable than the NI. Density was maximal in the lower cortex in 46% of gyri, in the upper cortical laminae in 8% of gyri, and a bimodal distribution in 15% of gyri. In the remaining gyri, there was a more even distribution of SN with cortical depth. In 31% of gyri, the vertical density of the NI was positively correlated with that of the SN. The data suggest that cortical degeneration in the temporal lobe of NID initially affects neurons in the lower laminae. Subsequently, the pathology may spread to affect much of the cortical profile, the SN preceding the appearance of the NI.
{"title":"Laminar distribution of neurofilament inclusions and swollen achromatic neurons in neurofilament inclusion disease (NID)","authors":"N. Cairns, E. Jaros, R. Perry, R. Armstrong","doi":"10.1002/NRC.20004","DOIUrl":"https://doi.org/10.1002/NRC.20004","url":null,"abstract":"The laminar distribution of the neurofilament inclusions (NI) and swollen achromatic neurons (SN) was studied in gyri of the temporal cortex in four patients with neurofilament inclusion disease (NID). In 84% of gyri analysed, the density of the NI was maximal in the lower cortical laminae. The distribution of the SN was more variable than the NI. Density was maximal in the lower cortex in 46% of gyri, in the upper cortical laminae in 8% of gyri, and a bimodal distribution in 15% of gyri. In the remaining gyri, there was a more even distribution of SN with cortical depth. In 31% of gyri, the vertical density of the NI was positively correlated with that of the SN. The data suggest that cortical degeneration in the temporal lobe of NID initially affects neurons in the lower laminae. Subsequently, the pathology may spread to affect much of the cortical profile, the SN preceding the appearance of the NI.","PeriodicalId":19198,"journal":{"name":"Neuroscience Research Communications","volume":"352 1","pages":"104-111"},"PeriodicalIF":0.0,"publicationDate":"2004-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"76396048","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}
Sung-Soo Kim, Mal-Soon Shin, Hong Kim, Eun-Kyung Kim, Hee-Hyuk Lee, Hyun-kyung Chang, Taeck-Hyun Lee, M. Jang, M. Shin, Baek-Vin Lim, Chang-Ju Kim
Exercise has been known to potentially affect food intake. Neuropeptide Y (NPY) is a 36 amino acid peptide and concentrated in the hypothalamus which is an appetite-regulating area. NPY is known to stimulate appetite and decrease energy expenditure. In the present study, the effect of treadmill running on the NPY expression in the hypothalamus of food-deprived rats was investigated using immunohistochemistry. Enhanced NPY expression in the paraventricular nucleus (PVN) and arcuate nucleus (ARN) was observed in the food-deprived rats. Treadmill exercise suppressed the enhancement of NPY expression in the PVN and ARN following food deprivation, but this suppressive effect was not affected by exercise intensity. Based on the present results, it can be suggested that treadmill exercise is effective in limiting the enhancement of NPY expression following food-deprived conditions.
{"title":"Treadmill exercise suppresses NPY expression in the hypothalamus of food-deprived rats","authors":"Sung-Soo Kim, Mal-Soon Shin, Hong Kim, Eun-Kyung Kim, Hee-Hyuk Lee, Hyun-kyung Chang, Taeck-Hyun Lee, M. Jang, M. Shin, Baek-Vin Lim, Chang-Ju Kim","doi":"10.1002/NRC.20001","DOIUrl":"https://doi.org/10.1002/NRC.20001","url":null,"abstract":"Exercise has been known to potentially affect food intake. Neuropeptide Y (NPY) is a 36 amino acid peptide and concentrated in the hypothalamus which is an appetite-regulating area. NPY is known to stimulate appetite and decrease energy expenditure. In the present study, the effect of treadmill running on the NPY expression in the hypothalamus of food-deprived rats was investigated using immunohistochemistry. Enhanced NPY expression in the paraventricular nucleus (PVN) and arcuate nucleus (ARN) was observed in the food-deprived rats. Treadmill exercise suppressed the enhancement of NPY expression in the PVN and ARN following food deprivation, but this suppressive effect was not affected by exercise intensity. Based on the present results, it can be suggested that treadmill exercise is effective in limiting the enhancement of NPY expression following food-deprived conditions.","PeriodicalId":19198,"journal":{"name":"Neuroscience Research Communications","volume":"9 1","pages":"63-71"},"PeriodicalIF":0.0,"publicationDate":"2004-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"77674677","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. Radenović, M. Jovanović, I. Vasiljević, V. Selaković
Glutamate neurotoxicity has been hypothesized to underlie several types of acute brain injury. Free radical reactions are implicated in a variety of physiological and pathological processes and abnormalities associated with superoxide dismutase (SOD) have been recently documented in several neurodegenerative processes. We investigated superoxide production and MnSOD activity after kainate injection into the CA3 region of the rat hippocampus. The measurements take place at different times in the hippocampus, forebrain cortex, straitum and cerebellum homogenates. Free radicals including superoxide are responsible for postlesional cytotoxicity. The increase of MnSOD in distinct brain regions, which are functionally connected via afferents and efferents, suggests that these regions are affected by the injury. It suggests that MnSOD protects the cells in these regions from superoxide-induced damage and therefore may limit the retrograde and anterograde spread of neurotoxicity.
{"title":"Superoxide production and the activity of MnSOD in rat brain after intrahippocampal kainate-induced seizure","authors":"L. Radenović, M. Jovanović, I. Vasiljević, V. Selaković","doi":"10.1002/NRC.20003","DOIUrl":"https://doi.org/10.1002/NRC.20003","url":null,"abstract":"Glutamate neurotoxicity has been hypothesized to underlie several types of acute brain injury. Free radical reactions are implicated in a variety of physiological and pathological processes and abnormalities associated with superoxide dismutase (SOD) have been recently documented in several neurodegenerative processes. We investigated superoxide production and MnSOD activity after kainate injection into the CA3 region of the rat hippocampus. The measurements take place at different times in the hippocampus, forebrain cortex, straitum and cerebellum homogenates. Free radicals including superoxide are responsible for postlesional cytotoxicity. The increase of MnSOD in distinct brain regions, which are functionally connected via afferents and efferents, suggests that these regions are affected by the injury. It suggests that MnSOD protects the cells in these regions from superoxide-induced damage and therefore may limit the retrograde and anterograde spread of neurotoxicity.","PeriodicalId":19198,"journal":{"name":"Neuroscience Research Communications","volume":"101 4 1","pages":"92-103"},"PeriodicalIF":0.0,"publicationDate":"2004-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"83329196","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}
Regulators of G-protein signaling family members, such as RGS2, are thought to primarily be involved in regulating the activity of second messenger systems by attenuating heterotrimeric G-protein actions. However, we found previously that RGS2 is predominantly located in the nucleus, not at the plasma membrane where most G-proteins exist, and that stressful conditions increased RGS2 expression. Here we report that induction of DNA damage-induced cell cycle arrest with camptothecin caused prolonged increases in RGS2, and decreases in RGS4, mRNA levels. Cell cycle arrest caused by nocodazole also increased RGS2, and decreased RGS4, mRNA levels. Additionally, using synchronization to minimize cell stress, RGS2 mRNA levels were low in G0 and G1, and elevated in the other phases of the cell cycle. These results demonstrate that RGS2 expression is coupled to cellular stress and the cell cycle, and that these conditions cause opposite effects on RGS2 and RGS4 mRNA levels.
{"title":"Stress‐ and cell cycle‐associated regulation of RGS2 mRNA levels","authors":"J. Zmijewski, Ling Song, R. Jope","doi":"10.1002/NRC.20000","DOIUrl":"https://doi.org/10.1002/NRC.20000","url":null,"abstract":"Regulators of G-protein signaling family members, such as RGS2, are thought to primarily be involved in regulating the activity of second messenger systems by attenuating heterotrimeric G-protein actions. However, we found previously that RGS2 is predominantly located in the nucleus, not at the plasma membrane where most G-proteins exist, and that stressful conditions increased RGS2 expression. Here we report that induction of DNA damage-induced cell cycle arrest with camptothecin caused prolonged increases in RGS2, and decreases in RGS4, mRNA levels. Cell cycle arrest caused by nocodazole also increased RGS2, and decreased RGS4, mRNA levels. Additionally, using synchronization to minimize cell stress, RGS2 mRNA levels were low in G0 and G1, and elevated in the other phases of the cell cycle. These results demonstrate that RGS2 expression is coupled to cellular stress and the cell cycle, and that these conditions cause opposite effects on RGS2 and RGS4 mRNA levels.","PeriodicalId":19198,"journal":{"name":"Neuroscience Research Communications","volume":"239 1","pages":"72-81"},"PeriodicalIF":0.0,"publicationDate":"2004-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"74697881","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 examined the effects of an aqueous-soluble carboxyfullerene analogue on the cerebral ischemia-induced infarct volume, and on extracellular glutamate accumulation, in an anesthetized rat brain cortex. A C3-symmetric carboxylic acid derivative of C60 (C3-C60), which contains three malonic acid groups per molecule, was administered intraventricularly (5 μL of a 30-μM solution of C3-C60 over a period of 40 min). Cerebral ischemia was induced by the ligation of bilateral common carotid arteries (CCA) and the unilateral middle cerebral artery (MCA). The infarct volume was calculated by analysis of 2-mm coronal sections of brain slices that were stained using TTC. We analyzed the glutamate concentrations in the cortex by microdialysis perfusion and on-line HPLC analysis. Administering C3-C60 significantly decreases the infarct volume (infarct percentage relative to total volume: 8 ± 1.4%) when compared with the vehicle (22 ± 2.6%; p < 0.01), which was similar to that of the control (22 ± 1.2%). Additionally, administering C3-C60 significantly decreases ischemia-induced extracellular glutamate accumulation when compared with the vehicle. These results suggest that an aqueous-soluble analogue of carboxyfullerene can protect a cerebral ischemia-induced infarct. This protective effect may be related to the attention of the accumulation of extracellular excitatory amino acids such as glutamate. The detailed mechanisms underlying the neuroprotective effects of C3-C60 require further investigation.
{"title":"Aqueous carboyxfullerene analogue attenuated cerebral infarct and extracellular glutamate levels in anesthetized rat","authors":"P. Tsai, Wenyin Chen, T. Luh, Chung S. Yang","doi":"10.1002/NRC.20005","DOIUrl":"https://doi.org/10.1002/NRC.20005","url":null,"abstract":"We have examined the effects of an aqueous-soluble carboxyfullerene analogue on the cerebral ischemia-induced infarct volume, and on extracellular glutamate accumulation, in an anesthetized rat brain cortex. A C3-symmetric carboxylic acid derivative of C60 (C3-C60), which contains three malonic acid groups per molecule, was administered intraventricularly (5 μL of a 30-μM solution of C3-C60 over a period of 40 min). Cerebral ischemia was induced by the ligation of bilateral common carotid arteries (CCA) and the unilateral middle cerebral artery (MCA). The infarct volume was calculated by analysis of 2-mm coronal sections of brain slices that were stained using TTC. We analyzed the glutamate concentrations in the cortex by microdialysis perfusion and on-line HPLC analysis. Administering C3-C60 significantly decreases the infarct volume (infarct percentage relative to total volume: 8 ± 1.4%) when compared with the vehicle (22 ± 2.6%; p < 0.01), which was similar to that of the control (22 ± 1.2%). Additionally, administering C3-C60 significantly decreases ischemia-induced extracellular glutamate accumulation when compared with the vehicle. These results suggest that an aqueous-soluble analogue of carboxyfullerene can protect a cerebral ischemia-induced infarct. This protective effect may be related to the attention of the accumulation of extracellular excitatory amino acids such as glutamate. The detailed mechanisms underlying the neuroprotective effects of C3-C60 require further investigation.","PeriodicalId":19198,"journal":{"name":"Neuroscience Research Communications","volume":"1 1","pages":"112-119"},"PeriodicalIF":0.0,"publicationDate":"2004-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"88877954","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}
B. Park, Ji Hyo Hwang, M. S. Kim, M. Lee, J. Rhee, S. Lee
To evaluate the effects of electrical stimulation of the sciatic nerve on brain-derived neurotrophic factor (BDNF) expression in the soleus and medial gastrocnemius muscles, we investigated temporal changes in BDNF protein and mRNA expression following electrical stimulation, and the optimal electrical stimulus paradigm for increasing BDNF expression in rats. The sciatic nerve was electrically stimulated with three different paradigms: 1 ms/40 Hz/30 min, 1 ms/40 Hz/40 Hz/5 min and 1 ms/1 Hz/30 min. Levels of BDNF protein and mRNA increased gradually over time after electrical stimulation in both muscles. Of the three stimulus paradigms, electrical stimulation at 1 ms/40 Hz/30 min produced the highest levels of BDNF protein and mRNA in both muscles, whereas stimulation at 1 ms/40 Hz/5 min produced the lowest expression levels. These results suggest that electrical stimulation could enhance neuronal plasticity by increasing BDNF production and paradigms of the stimulus can modulate the level of BDNF production.
{"title":"MODULATION OF BDNF EXPRESSION BY ELECTRICAL STIMULATION IN HINDLIMB MUSCLES OF RATS","authors":"B. Park, Ji Hyo Hwang, M. S. Kim, M. Lee, J. Rhee, S. Lee","doi":"10.1002/NRC.10101","DOIUrl":"https://doi.org/10.1002/NRC.10101","url":null,"abstract":"To evaluate the effects of electrical stimulation of the sciatic nerve on brain-derived neurotrophic factor (BDNF) expression in the soleus and medial gastrocnemius muscles, we investigated temporal changes in BDNF protein and mRNA expression following electrical stimulation, and the optimal electrical stimulus paradigm for increasing BDNF expression in rats. The sciatic nerve was electrically stimulated with three different paradigms: 1 ms/40 Hz/30 min, 1 ms/40 Hz/40 Hz/5 min and 1 ms/1 Hz/30 min. Levels of BDNF protein and mRNA increased gradually over time after electrical stimulation in both muscles. Of the three stimulus paradigms, electrical stimulation at 1 ms/40 Hz/30 min produced the highest levels of BDNF protein and mRNA in both muscles, whereas stimulation at 1 ms/40 Hz/5 min produced the lowest expression levels. These results suggest that electrical stimulation could enhance neuronal plasticity by increasing BDNF production and paradigms of the stimulus can modulate the level of BDNF production.","PeriodicalId":19198,"journal":{"name":"Neuroscience Research Communications","volume":"20 1","pages":"10-19"},"PeriodicalIF":0.0,"publicationDate":"2004-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"74020964","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}
Hyuk-Sang Jung, Hyun-Sam Lee, Jung-Won Shin, Doo-Jae Lee, R. Won, N. Sohn
Recent study has shown that whisker stimulation of intact whiskers causes c-Fos expression in contralateral barrel layers. However, as few reports have investigated what kind of effect whisker stimuli has on c-Fos expression in the ipsilateral cerebral cortex, we researched the effect of such whisker stimuli. One side of the whisker pad was deafferented on adult rats, so that the deafferented barrel no longer received direct external stimuli and only one side of the barrel-whisker system remained. Whiskers on the intact side were then stimulated and the effects of these stimuli on the ipsilateral deafferented barrel cortex were investigated by observing levels of c-Fos expression, which is known as an excellent marker for functionally excited neurons. Whisker stimulation caused significantly increased c-Fos expression on the layers II/III, IV of the ipsilateral deafferented cerebral cortex (P < 0.05, P < 0.01). In conclusion, whisker stimulation caused c-Fos expression not only in the contralateral cerebral cortex, but also in the ipsilateral cerebral cortex.
最近的研究表明，完整晶须的晶须刺激引起对侧桶状层中c-Fos的表达。然而，由于很少有报道研究须须刺激对同侧大脑皮层c-Fos表达的影响，我们研究了这种须须刺激的影响。对成年大鼠的须垫的一侧进行去神经化处理，使去神经化的桶不再接受直接的外部刺激，只保留了桶-须系统的一侧。然后刺激完整侧的须，并通过观察c-Fos表达水平来研究这些刺激对同侧失传入桶皮层的影响，c-Fos被认为是功能兴奋神经元的优秀标志。须刺激可显著提高同侧失传入脑皮层II/III、IV层c-Fos表达(P < 0.05, P < 0.01)。综上所述，须刺激不仅在对侧大脑皮层，而且在同侧大脑皮层也引起了c-Fos的表达。
{"title":"Does whisker stimulation induce c‐Fos expression in the rat ipsilateral deafferented cerebral cortex?","authors":"Hyuk-Sang Jung, Hyun-Sam Lee, Jung-Won Shin, Doo-Jae Lee, R. Won, N. Sohn","doi":"10.1002/NRC.10106","DOIUrl":"https://doi.org/10.1002/NRC.10106","url":null,"abstract":"Recent study has shown that whisker stimulation of intact whiskers causes c-Fos expression in contralateral barrel layers. However, as few reports have investigated what kind of effect whisker stimuli has on c-Fos expression in the ipsilateral cerebral cortex, we researched the effect of such whisker stimuli. One side of the whisker pad was deafferented on adult rats, so that the deafferented barrel no longer received direct external stimuli and only one side of the barrel-whisker system remained. Whiskers on the intact side were then stimulated and the effects of these stimuli on the ipsilateral deafferented barrel cortex were investigated by observing levels of c-Fos expression, which is known as an excellent marker for functionally excited neurons. Whisker stimulation caused significantly increased c-Fos expression on the layers II/III, IV of the ipsilateral deafferented cerebral cortex (P < 0.05, P < 0.01). In conclusion, whisker stimulation caused c-Fos expression not only in the contralateral cerebral cortex, but also in the ipsilateral cerebral cortex.","PeriodicalId":19198,"journal":{"name":"Neuroscience Research Communications","volume":"20 1","pages":"56-62"},"PeriodicalIF":0.0,"publicationDate":"2004-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"85720601","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}
Hyuk-Sang Jung, Hyun-Sam Lee, Jung-Won Shin, Doo-Jae Lee, R. Won, N. Sohn
A long-term study of a cerebral ischemia model, considered valuable in developing better treatments of ischemia, was performed to understand the nature of the dysfunctions associated with stroke. This study focused on the behavioral recovery and cognitive learning and memory of rats over a 17-week period following middle cerebral artery occlusion (MCAO). The present study involved the design of a comprehensive guideline for clinical behavior evaluation. The behavior of ischemic rats was examined over 17 weeks from 4 different aspects: posture & balance tests (4 subtests), reflex tests (6 subtests), muscle-tone tests (3 subtests), and a foot-fault test. After the tests, the results were analyzed to reveal the relationship between hemispheric atrophy and functional evaluation scores. Each battery of behavioral tests revealed multiple recovery phases in the time courses. Also, in the passive avoidance test, the MCAO group differed significantly from the sham group until 8 weeks, at which point the latencies to the sham group levels had occurred and after which there was no significant difference until 17 weeks. Thus, the present study provides a valuable protocol in long-term neuroprotection studies and presents an important profile of motor function that will supplement standard histopathological analysis at a later stage of ischemia.
{"title":"A long‐term locomotor function and cognition study following middle cerebral artery occlusion in rats","authors":"Hyuk-Sang Jung, Hyun-Sam Lee, Jung-Won Shin, Doo-Jae Lee, R. Won, N. Sohn","doi":"10.1002/NRC.10104","DOIUrl":"https://doi.org/10.1002/NRC.10104","url":null,"abstract":"A long-term study of a cerebral ischemia model, considered valuable in developing better treatments of ischemia, was performed to understand the nature of the dysfunctions associated with stroke. This study focused on the behavioral recovery and cognitive learning and memory of rats over a 17-week period following middle cerebral artery occlusion (MCAO). The present study involved the design of a comprehensive guideline for clinical behavior evaluation. The behavior of ischemic rats was examined over 17 weeks from 4 different aspects: posture & balance tests (4 subtests), reflex tests (6 subtests), muscle-tone tests (3 subtests), and a foot-fault test. After the tests, the results were analyzed to reveal the relationship between hemispheric atrophy and functional evaluation scores. Each battery of behavioral tests revealed multiple recovery phases in the time courses. Also, in the passive avoidance test, the MCAO group differed significantly from the sham group until 8 weeks, at which point the latencies to the sham group levels had occurred and after which there was no significant difference until 17 weeks. Thus, the present study provides a valuable protocol in long-term neuroprotection studies and presents an important profile of motor function that will supplement standard histopathological analysis at a later stage of ischemia.","PeriodicalId":19198,"journal":{"name":"Neuroscience Research Communications","volume":"63 1","pages":"37-46"},"PeriodicalIF":0.0,"publicationDate":"2004-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"80872955","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}
E. Odacı, S. Kaplan, B. Sahin, O. Baş, F. Gevrek, D. Aygün, B. Unal, O. Sonmez, S. Çolakoğlu, S. Bilgiç
SUMMARY Oxcarbazepine (OXC) is a widely used novel antiepileptic drug that has been available for routine prescription for 10 years. To examine low dose OXC-induced neurotoxic effects on cerebellar development, we administered 25 mg/kg OXC orally to newborn Wistar rats once a day on postnatal days 2-14. Microscopic processed cerebellar sections of the control and treated groups were examined by volumetric analysis. Volume estimations were obtained using the Cavalieri’s principle using a computerized stereological image analyzer (CAST-GRID). The total volume of the cerebellum, white matter and the various cerebellar layers (except extragranular layer) were significantly increased in the treated animals. These data may provide useful implications for the management of OXC-induced developmental neurotoxicity in children exposed to OXC during the late fetal period. Our finings suggest that women suffering from epilepsy should be given OXC carefully only at the lowest effective doses during pregnancy.
{"title":"Effects of low‐dose oxcarbazepine administration on developing cerebellum in newborn rat: A stereological study","authors":"E. Odacı, S. Kaplan, B. Sahin, O. Baş, F. Gevrek, D. Aygün, B. Unal, O. Sonmez, S. Çolakoğlu, S. Bilgiç","doi":"10.1002/NRC.10103","DOIUrl":"https://doi.org/10.1002/NRC.10103","url":null,"abstract":"SUMMARY Oxcarbazepine (OXC) is a widely used novel antiepileptic drug that has been available for routine prescription for 10 years. To examine low dose OXC-induced neurotoxic effects on cerebellar development, we administered 25 mg/kg OXC orally to newborn Wistar rats once a day on postnatal days 2-14. Microscopic processed cerebellar sections of the control and treated groups were examined by volumetric analysis. Volume estimations were obtained using the Cavalieri’s principle using a computerized stereological image analyzer (CAST-GRID). The total volume of the cerebellum, white matter and the various cerebellar layers (except extragranular layer) were significantly increased in the treated animals. These data may provide useful implications for the management of OXC-induced developmental neurotoxicity in children exposed to OXC during the late fetal period. Our finings suggest that women suffering from epilepsy should be given OXC carefully only at the lowest effective doses during pregnancy.","PeriodicalId":19198,"journal":{"name":"Neuroscience Research Communications","volume":"18 1","pages":"28-36"},"PeriodicalIF":0.0,"publicationDate":"2004-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"82840318","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}
B. Unal, M. Özbek, Aydin, N. Aydın, Z. Bulucu, Ozgen Vuraler, E. Odacı, B. Sahin, S. Kaplan
In recent studies, some neuroleptics have shown neurotoxic activities. Clinical and experimental studies have been carried out to investigate the effects of different neuroleptic drugs considered to affect the central nervous system. The aim of this study was to evaluate neurotoxic effects of halperidol on hippocampal neurons. The drug was given in daily doses of either 1 or 3 mg/kg for 6 weeks to adult male guinea pigs. After treatment, all animals were anaesthetized via short inhalation of ether, and then were fixed by a mixture of 2% glutaraldehyde and +2% paraformaldehyde in 0.1 M phosphate buffer. Brains were removed from the cranium and stored in the same fixative overnight. On the following day, the CA1 region of the hippocampus was dissected out. After embedding in araldite resin and obtaining semi-thin sections, the tissues were stained with toluidine blue. The physical dissector was used for measurements of nuclear height and numerical density of neurons and the sections were also evaluated histopathologically. The numerical density of neurons and nuclear height in the hippocampus for the low-dose (1 mg/kg) and high-dose (3 mg/kg) experimental groups were 12.4 mm3 and 3.6 μm and 7.14 mm3 and 3.56 μm, respectively. In contrast, the control group had a neuronal numerical density of 16.55 mm −3 and a nuclear height of 4.09 μm. There was a significant difference in both the mean density of neurons and the mean height of nuclei between haloperidol-treated and control groups (p < 0.05). There was also a statistical difference in the mean density of neurons (but not in nuclear height) when comparing the dosage of haloperidol (p < 0.05). These findings suggest that haloperidol treatment may lead to a loss of neurons as well as a decrease in the height of nuclei in the hippocampus.
{"title":"Effect of haloperidol on the numeric density of neurons and nuclear height in the rat hippocampus: A stereological and histopathological study","authors":"B. Unal, M. Özbek, Aydin, N. Aydın, Z. Bulucu, Ozgen Vuraler, E. Odacı, B. Sahin, S. Kaplan","doi":"10.1002/NRC.10100","DOIUrl":"https://doi.org/10.1002/NRC.10100","url":null,"abstract":"In recent studies, some neuroleptics have shown neurotoxic activities. Clinical and experimental studies have been carried out to investigate the effects of different neuroleptic drugs considered to affect the central nervous system. The aim of this study was to evaluate neurotoxic effects of halperidol on hippocampal neurons. The drug was given in daily doses of either 1 or 3 mg/kg for 6 weeks to adult male guinea pigs. After treatment, all animals were anaesthetized via short inhalation of ether, and then were fixed by a mixture of 2% glutaraldehyde and +2% paraformaldehyde in 0.1 M phosphate buffer. Brains were removed from the cranium and stored in the same fixative overnight. On the following day, the CA1 region of the hippocampus was dissected out. After embedding in araldite resin and obtaining semi-thin sections, the tissues were stained with toluidine blue. The physical dissector was used for measurements of nuclear height and numerical density of neurons and the sections were also evaluated histopathologically. The numerical density of neurons and nuclear height in the hippocampus for the low-dose (1 mg/kg) and high-dose (3 mg/kg) experimental groups were 12.4 mm3 and 3.6 μm and 7.14 mm3 and 3.56 μm, respectively. In contrast, the control group had a neuronal numerical density of 16.55 mm −3 and a nuclear height of 4.09 μm. There was a significant difference in both the mean density of neurons and the mean height of nuclei between haloperidol-treated and control groups (p < 0.05). There was also a statistical difference in the mean density of neurons (but not in nuclear height) when comparing the dosage of haloperidol (p < 0.05). These findings suggest that haloperidol treatment may lead to a loss of neurons as well as a decrease in the height of nuclei in the hippocampus.","PeriodicalId":19198,"journal":{"name":"Neuroscience Research Communications","volume":"24 1","pages":"1-9"},"PeriodicalIF":0.0,"publicationDate":"2004-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"84847121","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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