Eun-Kyung Kim, Hong Kim, Myoung-Hwa Lee, Y. S. Kim, Hye-Young Yang, Hyun-kyung Chang, Taeck-Hyun Lee, M. Jang, M. Shin, S. Lee, Hee-Hyuk Lee, Mal-Soon Shin, Chang-Ju Kim
During the prenatal period, development of individual is influenced by the environmental factors. In mammals, 5-hydroxytryptamine (5-HT) is a central neurotransmitter that regulates behavioral functions in the vertebrate brain. Tryptophan hydroxylase (TPH) is a rate-limiting enzyme in the 5-HT synthesis. Various stresses are known to modulate the 5-HT synthesis and the TPH expression. In the present study, the influence of prenatal noise and music aplication on the 5-HT synthesis and the TPH expression in the dorsal and median raphe of young rats was investigated. Prenatal noise application increased the 5-HT synthesis and the TPH expression in the dorsal and median raphe nuclei of offspring. Prenatal music application, in contrast, decreased the 5-HT synthesis and the TPH expression in the dorsal and median raphe nuclei of offspring. The present study suggests that prenatal stimuli including noise and music may affect the emotional state of offspring.
{"title":"Influence of prenatal noise and music on the 5-hydroxytryptamine synthesis and the tryptophan hydroxylase expression in the raphe nuclei of young rats","authors":"Eun-Kyung Kim, Hong Kim, Myoung-Hwa Lee, Y. S. Kim, Hye-Young Yang, Hyun-kyung Chang, Taeck-Hyun Lee, M. Jang, M. Shin, S. Lee, Hee-Hyuk Lee, Mal-Soon Shin, Chang-Ju Kim","doi":"10.1002/NRC.20026","DOIUrl":"https://doi.org/10.1002/NRC.20026","url":null,"abstract":"During the prenatal period, development of individual is influenced by the environmental factors. In mammals, 5-hydroxytryptamine (5-HT) is a central neurotransmitter that regulates behavioral functions in the vertebrate brain. Tryptophan hydroxylase (TPH) is a rate-limiting enzyme in the 5-HT synthesis. Various stresses are known to modulate the 5-HT synthesis and the TPH expression. In the present study, the influence of prenatal noise and music aplication on the 5-HT synthesis and the TPH expression in the dorsal and median raphe of young rats was investigated. Prenatal noise application increased the 5-HT synthesis and the TPH expression in the dorsal and median raphe nuclei of offspring. Prenatal music application, in contrast, decreased the 5-HT synthesis and the TPH expression in the dorsal and median raphe nuclei of offspring. The present study suggests that prenatal stimuli including noise and music may affect the emotional state of offspring.","PeriodicalId":19198,"journal":{"name":"Neuroscience Research Communications","volume":"27 1","pages":"118-129"},"PeriodicalIF":0.0,"publicationDate":"2004-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"81430957","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}
Two cytoprotective agents, ethiofos (WR2721) and nerve growth factor (NGF), were used to diminish cisplatin-induced toxicity in Schwann cell cultures. The effect of both studied agents was estimated by a micronucleus test and the comet assay. The comet assay was performed in cultured human Schwann cells isolated from sural nerve biopsies, and the micronucleus test was used in primary cultures of Schwann cells isolated from foetal rat dorsal root ganglia (DRG). A dose-dependent increase in the number of cells displaying DNA damage was found at both concentrations of cisplatin, 0.5 and 1.0 μM. No significant protective effect of either β-NGF or WR-2721 was observed in human Schwann cell cultures. A significant protective effect was obtained in the cultures of Schwann cells isolated from foetal rat DRG, when treated simultaneously with 0.5 μM cisplatin and 10 ng/ml β-NGF. WR-2721 was not effective in these cells.
{"title":"Effect of two different cytoprotectives, ethiofos and β-NGF, on cisplatin-induced toxicity in Schwann cell cultures; a preliminary study","authors":"K. Jirsova, V. Mandys, P. Bär","doi":"10.1002/NRC.20024","DOIUrl":"https://doi.org/10.1002/NRC.20024","url":null,"abstract":"Two cytoprotective agents, ethiofos (WR2721) and nerve growth factor (NGF), were used to diminish cisplatin-induced toxicity in Schwann cell cultures. The effect of both studied agents was estimated by a micronucleus test and the comet assay. The comet assay was performed in cultured human Schwann cells isolated from sural nerve biopsies, and the micronucleus test was used in primary cultures of Schwann cells isolated from foetal rat dorsal root ganglia (DRG). A dose-dependent increase in the number of cells displaying DNA damage was found at both concentrations of cisplatin, 0.5 and 1.0 μM. No significant protective effect of either β-NGF or WR-2721 was observed in human Schwann cell cultures. A significant protective effect was obtained in the cultures of Schwann cells isolated from foetal rat DRG, when treated simultaneously with 0.5 μM cisplatin and 10 ng/ml β-NGF. WR-2721 was not effective in these cells.","PeriodicalId":19198,"journal":{"name":"Neuroscience Research Communications","volume":"25 1","pages":"96-104"},"PeriodicalIF":0.0,"publicationDate":"2004-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"82844671","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}
Jong‐Seong Park, H. Jeong, Tae‐Sun Kim, Yo-Sik Kim, Jae-Ha Kim, Myung-Joo Jang, Ja-Yeon Kim, Mei Huang
The aim of this study is to explore the action of 5-HT1 receptor on spontaneous firing activity of the rat medial vestibular nuclear neurons by patch clamp experiments. The spontaneous firing was increased in 45.5% and decreased in 54.5% of the neurons tested with 5-carboxamidotryptamine, non-selective 5-HT1 receptor agonist. And the whole potassium currents of medial vestibular nuclear neurons was decreased in 64% and increased in 36% of cells tested with 5-carboxamidotryptamine. The spontaneous firing rate was increased by 8-OH-DPAT, selective 5-HT1A receptor agonist in 73.3% and was not changed in 26.7%. Whole potassium currents were decreased in 84.2% and was not affected in 15.8% by 8-OH-DPAT. These results suggest that 5-HTIA receptor of the medial vestibular nuclear neurons mediates excitatory effects whereas inhibitory effects are mediated by other 5-HT1 receptors.
{"title":"Effects of 5‐HT1 receptor agonist on the excitability of medial vestibular nuclear neurons","authors":"Jong‐Seong Park, H. Jeong, Tae‐Sun Kim, Yo-Sik Kim, Jae-Ha Kim, Myung-Joo Jang, Ja-Yeon Kim, Mei Huang","doi":"10.1002/NRC.20028","DOIUrl":"https://doi.org/10.1002/NRC.20028","url":null,"abstract":"The aim of this study is to explore the action of 5-HT1 receptor on spontaneous firing activity of the rat medial vestibular nuclear neurons by patch clamp experiments. The spontaneous firing was increased in 45.5% and decreased in 54.5% of the neurons tested with 5-carboxamidotryptamine, non-selective 5-HT1 receptor agonist. And the whole potassium currents of medial vestibular nuclear neurons was decreased in 64% and increased in 36% of cells tested with 5-carboxamidotryptamine. The spontaneous firing rate was increased by 8-OH-DPAT, selective 5-HT1A receptor agonist in 73.3% and was not changed in 26.7%. Whole potassium currents were decreased in 84.2% and was not affected in 15.8% by 8-OH-DPAT. These results suggest that 5-HTIA receptor of the medial vestibular nuclear neurons mediates excitatory effects whereas inhibitory effects are mediated by other 5-HT1 receptors.","PeriodicalId":19198,"journal":{"name":"Neuroscience Research Communications","volume":"176 1","pages":"139-149"},"PeriodicalIF":0.0,"publicationDate":"2004-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"79826153","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. Armstrong, Elena Paik, S. Chhith, V. Lelièvre, J. Waschek, S. Howard
To elucidate the role of the serotonin (5-HT)2A/2C receptors in 3,4-methylenedioxymethamphetamine (MDMA)-induced neurotoxicity, MDMA was administered to rats and the presence of the serotonin transporter (5-HTT) was assessed at the protein level with immunohistochemistry (IHC), and the RNA level with a Northern blotting technique. d-lysergic acid diethylamide (LSD) and MDL 11,939 were given in conjunction with MDMA in order to assess the importance of 5-HT receptors in MDMA-induced neurotoxicity. The hypothesis is that the MDMA + LSD-treated animals should have more neurotoxicity as measured by loss of 5-HTTs compared to the MDMA-treated animals. Moreover, the loss of 5-HTTs should be attenuated in animals given the combination of MDMA + MDL 11,939, as the latter drug is a selective 5-HT2A/2C antagonist. The results showed that MDMA-induced neurotoxicity was dose dependently increased by LSD. Moreover, the drug MDL 11,939 attenuated MDMA-induced neurotoxicity, suggesting that 5-HT2A/2C receptors are involved in MDMA-induced neurotoxicity.
{"title":"Potentiation of (DL)‐3,4‐methylenedioxymethamphetamine (MDMA)‐induced toxicity by the serotonin 2A receptior partial agonist d‐lysergic acid diethylamide (LSD), and the protection of same by the serotonin 2A/2C receptor antagonist MDL 11,939","authors":"B. Armstrong, Elena Paik, S. Chhith, V. Lelièvre, J. Waschek, S. Howard","doi":"10.1002/NRC.20023","DOIUrl":"https://doi.org/10.1002/NRC.20023","url":null,"abstract":"To elucidate the role of the serotonin (5-HT)2A/2C receptors in 3,4-methylenedioxymethamphetamine (MDMA)-induced neurotoxicity, MDMA was administered to rats and the presence of the serotonin transporter (5-HTT) was assessed at the protein level with immunohistochemistry (IHC), and the RNA level with a Northern blotting technique. d-lysergic acid diethylamide (LSD) and MDL 11,939 were given in conjunction with MDMA in order to assess the importance of 5-HT receptors in MDMA-induced neurotoxicity. The hypothesis is that the MDMA + LSD-treated animals should have more neurotoxicity as measured by loss of 5-HTTs compared to the MDMA-treated animals. Moreover, the loss of 5-HTTs should be attenuated in animals given the combination of MDMA + MDL 11,939, as the latter drug is a selective 5-HT2A/2C antagonist. The results showed that MDMA-induced neurotoxicity was dose dependently increased by LSD. Moreover, the drug MDL 11,939 attenuated MDMA-induced neurotoxicity, suggesting that 5-HT2A/2C receptors are involved in MDMA-induced neurotoxicity.","PeriodicalId":19198,"journal":{"name":"Neuroscience Research Communications","volume":"495 1","pages":"83-95"},"PeriodicalIF":0.0,"publicationDate":"2004-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"77812697","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}
Hypothermia has a neuroprotective effect in cerebral ischemia and reduces brain edema, and decompressive craniectomy (DC) can prevent brain herniation caused by massive brain edema. Thus, combination of the two therapies may be more effective in large hemispheric infarctions, by exerting an additive effect. We investigated the effects of DC, hypothermia, and their combination in experimental cerebral ischemia. Seventy rats received focal cerebral ischemia for 72 hours and were allocated to one of four groups: untreated control (n=29), DC (n=21), hypothermia (n=10), and DC plus hypothermia (n=10). Hypothermia (34°C) and/or DC were performed 6 hours after ischemia. Mortality was 44.8% (control), 28.6% (DC), 10.0% (hypothermia), and 0% (DC plus hypothermia), respectively (p 0.1) but was by hypothermia (117.8±50.7 mm3), p<0.01). Although hypothermia combined with DC reduced the size of the infarction significantly (99.6±71.2 mm3), no additional effect was observed versus hypothermia alone.
{"title":"Effects of decompressive craniectomy, hypothermia and their combination in a permanent focal cerebral ischemia model","authors":"Ja-seong Koo, Y. Kim, B. Yoon","doi":"10.1002/NRC.20022","DOIUrl":"https://doi.org/10.1002/NRC.20022","url":null,"abstract":"Hypothermia has a neuroprotective effect in cerebral ischemia and reduces brain edema, and decompressive craniectomy (DC) can prevent brain herniation caused by massive brain edema. Thus, combination of the two therapies may be more effective in large hemispheric infarctions, by exerting an additive effect. We investigated the effects of DC, hypothermia, and their combination in experimental cerebral ischemia. Seventy rats received focal cerebral ischemia for 72 hours and were allocated to one of four groups: untreated control (n=29), DC (n=21), hypothermia (n=10), and DC plus hypothermia (n=10). Hypothermia (34°C) and/or DC were performed 6 hours after ischemia. Mortality was 44.8% (control), 28.6% (DC), 10.0% (hypothermia), and 0% (DC plus hypothermia), respectively (p 0.1) but was by hypothermia (117.8±50.7 mm3), p<0.01). Although hypothermia combined with DC reduced the size of the infarction significantly (99.6±71.2 mm3), no additional effect was observed versus hypothermia alone.","PeriodicalId":19198,"journal":{"name":"Neuroscience Research Communications","volume":"41 1","pages":"73-82"},"PeriodicalIF":0.0,"publicationDate":"2004-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"88622360","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
In the present study, we identified the key protein that modulates the initiation of functional glutamatergic synapses in developing cortical neurons. First, we found a day in vitro that marked a critical increase in the number of functional synapses by the application of cyclic AMP, as demonstrated with Ca2+ imaging. We then examined the changes in the expression levels of proteins, which were expected to play a role in glutamatergic synapses, by the application of cyclic AMP. Our findings suggest that the expression of the α-amino-3-hydroxy-5-methyl-4-isoxazole proprionic acid (AMPA) receptors modulates the initiation of functional synapses in developing neurons, and that immature neurons already contain N-methyl d-aspartate (NMDA) receptors and presynaptic proteins such as synaptophysin.
{"title":"Initiation of functional synapses is associated with AMPA receptor expression","authors":"K. Chono, H. Shiga, T. Tojima, E. Ito","doi":"10.1002/NRC.20016","DOIUrl":"https://doi.org/10.1002/NRC.20016","url":null,"abstract":"In the present study, we identified the key protein that modulates the initiation of functional glutamatergic synapses in developing cortical neurons. First, we found a day in vitro that marked a critical increase in the number of functional synapses by the application of cyclic AMP, as demonstrated with Ca2+ imaging. We then examined the changes in the expression levels of proteins, which were expected to play a role in glutamatergic synapses, by the application of cyclic AMP. Our findings suggest that the expression of the α-amino-3-hydroxy-5-methyl-4-isoxazole proprionic acid (AMPA) receptors modulates the initiation of functional synapses in developing neurons, and that immature neurons already contain N-methyl d-aspartate (NMDA) receptors and presynaptic proteins such as synaptophysin.","PeriodicalId":19198,"journal":{"name":"Neuroscience Research Communications","volume":"161 1","pages":"24-31"},"PeriodicalIF":0.0,"publicationDate":"2004-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"83166282","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}
Vascular disease probably plays an important role in the pathogenesis of cerebral complications that are associated with diabetes mellitus. Previous studies showed that treatment with the angiotensin converting enzyme-inhibitor enalapril (24 mg/kg) prevented neurophysiological and cognitive deficits in streptozotocin diabetic rats, and improved cerebral blood flow, despite a reduction in systemic mean arterial blood pressure. The present study examined if these effects could be sustained with long-term treatment, and if treatment with a lower dose (12 mg/kg) could prevent peripheral and central neurophysiological deficits without causing hypotension. Sciatic nerve conduction velocities were measured every three weeks after diabetes induction, until 24 weeks. Brain stem auditory (BAEP) and visual evoked potentials (VEP) were measured every three weeks from 10 weeks after diabetes induction, until 25 weeks. Nerve conduction velocity was decreased, and BAEP and VEP latencies increased in untreated diabetic rats. At the end of follow-up 12 mg/kg enalapril partially prevented evoked potential abnormalities, but not nerve conduction deficits, whereas 24 mg/kg enalapril largely prevented deficits in nerve conduction velocity (p<0.001), as well as BAEP (p<01) and VEP latencies (p<0.05). Mean arterial blood pressure was 122 mmHg in the untreated diabetic group, 75 mmHg in the 24 mg/kg group and 112 mmHg in the 12 mg/kg group. Sustained treatment with enalapril at 24 mg/kg was associated with increased mortality, which may be related to the marked hypotension at this dosage. We conclude that long-term treatment with enalapril at a dose of 24 mg/kg can prevent peripheral and central neurophysiological deficits in streptozotocin diabetic rats, but that adverse effects preclude sustained treatment.
{"title":"Long‐term angiotensin converting enzyme inhibition dose‐dependently improves nerve conduction velocity and evoked potential latencies in streptozotocin‐diabetic rats","authors":"S. Manschot, L. Kappelle, W. Gispen, G. Biessels","doi":"10.1002/NRC.20019","DOIUrl":"https://doi.org/10.1002/NRC.20019","url":null,"abstract":"Vascular disease probably plays an important role in the pathogenesis of cerebral complications that are associated with diabetes mellitus. Previous studies showed that treatment with the angiotensin converting enzyme-inhibitor enalapril (24 mg/kg) prevented neurophysiological and cognitive deficits in streptozotocin diabetic rats, and improved cerebral blood flow, despite a reduction in systemic mean arterial blood pressure. The present study examined if these effects could be sustained with long-term treatment, and if treatment with a lower dose (12 mg/kg) could prevent peripheral and central neurophysiological deficits without causing hypotension. Sciatic nerve conduction velocities were measured every three weeks after diabetes induction, until 24 weeks. Brain stem auditory (BAEP) and visual evoked potentials (VEP) were measured every three weeks from 10 weeks after diabetes induction, until 25 weeks. Nerve conduction velocity was decreased, and BAEP and VEP latencies increased in untreated diabetic rats. At the end of follow-up 12 mg/kg enalapril partially prevented evoked potential abnormalities, but not nerve conduction deficits, whereas 24 mg/kg enalapril largely prevented deficits in nerve conduction velocity (p<0.001), as well as BAEP (p<01) and VEP latencies (p<0.05). Mean arterial blood pressure was 122 mmHg in the untreated diabetic group, 75 mmHg in the 24 mg/kg group and 112 mmHg in the 12 mg/kg group. Sustained treatment with enalapril at 24 mg/kg was associated with increased mortality, which may be related to the marked hypotension at this dosage. We conclude that long-term treatment with enalapril at a dose of 24 mg/kg can prevent peripheral and central neurophysiological deficits in streptozotocin diabetic rats, but that adverse effects preclude sustained treatment.","PeriodicalId":19198,"journal":{"name":"Neuroscience Research Communications","volume":"64 1","pages":"51-62"},"PeriodicalIF":0.0,"publicationDate":"2004-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"78158561","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}
Sangho Kim, Hong Kim, Sung-Soo Kim, Mal-Soon Shin, Hyun-kyung Chang, Taeck-Hyun Lee, M. Jang, M. Shin, Hee-Hyuk Lee, Young Pyo Kim, Chang-Ju Kim
c-Fos has been used as a neuronal activity marker. Here, we examined the influence of age on the treadmill running-induced c-Fos expression in rat hippocampus. Rats of exercise groups were forces to run on treadmill for 30 min. once a day for 5 consecutive days. Without exercise, c-Fos expression was highest in 8-week old rats. Treadmill exercise significantly enhanced the c-Fos expression in the hippocampus of rats in all ages. In the CA region, the increase of the c-Fos expression by treadmill exercise was highest in 4-week old rats. In the dentate gyrus, the increase of the c-Fos expression by treadmill exercise was highest in 62-week old rats. The data show that age is an important factor for the regulation of the c-Fos expression in the hippocampus and that the ability of the treadmill exercise enhancing the c-Fos expression is dependent on age status.
{"title":"The influence of age on the treadmill exercise‐induced c‐Fos expression in the hippocampus of rats","authors":"Sangho Kim, Hong Kim, Sung-Soo Kim, Mal-Soon Shin, Hyun-kyung Chang, Taeck-Hyun Lee, M. Jang, M. Shin, Hee-Hyuk Lee, Young Pyo Kim, Chang-Ju Kim","doi":"10.1002/NRC.20018","DOIUrl":"https://doi.org/10.1002/NRC.20018","url":null,"abstract":"c-Fos has been used as a neuronal activity marker. Here, we examined the influence of age on the treadmill running-induced c-Fos expression in rat hippocampus. Rats of exercise groups were forces to run on treadmill for 30 min. once a day for 5 consecutive days. Without exercise, c-Fos expression was highest in 8-week old rats. Treadmill exercise significantly enhanced the c-Fos expression in the hippocampus of rats in all ages. In the CA region, the increase of the c-Fos expression by treadmill exercise was highest in 4-week old rats. In the dentate gyrus, the increase of the c-Fos expression by treadmill exercise was highest in 62-week old rats. The data show that age is an important factor for the regulation of the c-Fos expression in the hippocampus and that the ability of the treadmill exercise enhancing the c-Fos expression is dependent on age status.","PeriodicalId":19198,"journal":{"name":"Neuroscience Research Communications","volume":"63 1","pages":"41-50"},"PeriodicalIF":0.0,"publicationDate":"2004-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"88912060","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}
D. Hatakeyama, S. Inamura, E. Ito, M. Sakakibara, T. Nelson, D. Alkon
Calexcitin (CE) is a low molecular weight Ca2+- and guanosine triphosphate- binding protein, which is phosphorylated during associative learning in both vertebrates and invertebrates. The purpose of this study was to determine the presence of CE in the central nervous system (CNS) of the pond snail Lymnaea stagnalis, which can acquire classical and operant conditioning. Immunoblotting of CE showed that the anti-CE antibody prepared from squid can detect Lymnaea CE. In the cerebral ganglia, CE-like immunoreactivity was exhibited in two pairs of cell clusters that receive taste signals from the superior or median lip nerves. In both pedal ganglia, CE-like immunoreactivity was detected in 1-4 cell of the PeA clusters, which are involved in the withdrawal response. Our results therefore showed that CE is involved in the feeding and withdrawal neural networks, suggesting that CE may function in associative learning of feeding and withdrawal behavior in L. stagnalis.
{"title":"Calexcitin-like immunoreactivity in the pond snail Lymnaea stagnalis","authors":"D. Hatakeyama, S. Inamura, E. Ito, M. Sakakibara, T. Nelson, D. Alkon","doi":"10.1002/NRC.20017","DOIUrl":"https://doi.org/10.1002/NRC.20017","url":null,"abstract":"Calexcitin (CE) is a low molecular weight Ca2+- and guanosine triphosphate- binding protein, which is phosphorylated during associative learning in both vertebrates and invertebrates. The purpose of this study was to determine the presence of CE in the central nervous system (CNS) of the pond snail Lymnaea stagnalis, which can acquire classical and operant conditioning. Immunoblotting of CE showed that the anti-CE antibody prepared from squid can detect Lymnaea CE. In the cerebral ganglia, CE-like immunoreactivity was exhibited in two pairs of cell clusters that receive taste signals from the superior or median lip nerves. In both pedal ganglia, CE-like immunoreactivity was detected in 1-4 cell of the PeA clusters, which are involved in the withdrawal response. Our results therefore showed that CE is involved in the feeding and withdrawal neural networks, suggesting that CE may function in associative learning of feeding and withdrawal behavior in L. stagnalis.","PeriodicalId":19198,"journal":{"name":"Neuroscience Research Communications","volume":"22 1","pages":"32-40"},"PeriodicalIF":0.0,"publicationDate":"2004-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"80517325","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}
J. Tanaka, H. Miyakubo, Shigeko Fujisawa, M. Nomura
Previous studies have demonstrated that estrogen alters the responsiveness of subfornical organ (SFO) neurons projecting to the hypothalamic paraventricular nucleus (PVN) to angiotensin II (ANG II) and activation of the SFO facilitates noradrenaline (NA) release in the PVN area. The present study was carried out to investigate whether estrogen elicits alterations in the NA release in the PVN area induced by electrical and chemical activation of the SFO. Intracerebral microdialysis techniques were utilized to quantify the extracellular content of NA in the region of the PVN in ovariectomized (OVX) female rats that were treated with either propylene glycol (PG) vehicle or estradiol benzoate (EB). In both groups, electrical stimulation (5–20 Hz, 600 μA) of the SFO significantly increased the NA concentration in the PVN area. Injections of ANG II (10–8 M, 0.2 μl) into the stimulation site significantly enhanced the release of NA in the PVN area. The NA release to either electrical or chemical stimulation of the SFO was much greater in the PG-treated than in the EB-treated rats. These results suggest that estrogen may decrease the NA release in the PVN area caused by ANG II acting at the SFO.
先前的研究表明，雌激素改变下丘脑室旁核(PVN)投射的皮质下器官(SFO)神经元对血管紧张素II (ANG II)的反应性，SFO的激活促进PVN区域去甲肾上腺素(NA)的释放。本研究旨在探讨雌激素是否会引起SFO的电和化学激活引起PVN区域NA释放的改变。采用脑内微透析技术，定量测定经丙二醇(PG)或苯甲酸雌二醇(EB)处理的去卵巢雌性大鼠PVN区域NA的细胞外含量。两组SFO电刺激(5 ~ 20 Hz, 600 μA)均显著增加PVN区NA浓度。刺激部位注射ANG II (10-8 M, 0.2 μl)可显著促进PVN区NA的释放。与eb处理的大鼠相比，pg处理的大鼠在SFO的电或化学刺激下释放的NA要大得多。提示雌激素可减少ANG II作用于SFO引起的PVN区NA释放。
{"title":"Attenuated noradrenaline release in the paraventricular nucleus are induced by electrical and angiotensin II activation of the subfornical organ in estrogen‐treated rats","authors":"J. Tanaka, H. Miyakubo, Shigeko Fujisawa, M. Nomura","doi":"10.1002/NRC.20020","DOIUrl":"https://doi.org/10.1002/NRC.20020","url":null,"abstract":"Previous studies have demonstrated that estrogen alters the responsiveness of subfornical organ (SFO) neurons projecting to the hypothalamic paraventricular nucleus (PVN) to angiotensin II (ANG II) and activation of the SFO facilitates noradrenaline (NA) release in the PVN area. The present study was carried out to investigate whether estrogen elicits alterations in the NA release in the PVN area induced by electrical and chemical activation of the SFO. Intracerebral microdialysis techniques were utilized to quantify the extracellular content of NA in the region of the PVN in ovariectomized (OVX) female rats that were treated with either propylene glycol (PG) vehicle or estradiol benzoate (EB). In both groups, electrical stimulation (5–20 Hz, 600 μA) of the SFO significantly increased the NA concentration in the PVN area. Injections of ANG II (10–8 M, 0.2 μl) into the stimulation site significantly enhanced the release of NA in the PVN area. The NA release to either electrical or chemical stimulation of the SFO was much greater in the PG-treated than in the EB-treated rats. These results suggest that estrogen may decrease the NA release in the PVN area caused by ANG II acting at the SFO.","PeriodicalId":19198,"journal":{"name":"Neuroscience Research Communications","volume":"16 1","pages":"63-71"},"PeriodicalIF":0.0,"publicationDate":"2004-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"87000791","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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