Pub Date : 2015-01-10DOI: 10.2174/1874082001408010014
Kevin Joseph, R. Varatharajan, Sonya Neto, U. Hofmann, V. Tronnier, A. Moser
Electrical high frequency stimulation (HFS) in the subthalamic nucleus (STN) has been shown to have a thera- peutic effect in several movement disorders. But, debilitating psychiatric effects like depression and suicidality are occa- sionally seen and might be caused by the changes in the serotoninergic activity. Previous studies could show that HFS of the STN results in inhibition of the serotonergic neurons originating in the dorsal raphe nucleus. The aim of this study was to characterize the effect of HFS (124 Hz, 0.5 mA) in the STN, on the extracellular levels of serotonin, dopamine and their metabolites HIAA, DOPAC and HVA in the caudate-putamen (CPu) in conscious and freely moving rats. Extracellular levels of the neurotransmitters and their metabolites were quantified using high performance liquid chromatography with electrochemical detection. Under HFS conditions, a significant reduction in the extracellular levels of serotonin was ob- served. Cessation of HFS showed a recovery back to basal levels. Dopamine levels were not affected, although significant increase of its metabolites DOPAC and HVA were measured. In the case of low frequency stimulation (LFS), levels of se- rotonin and its metabolite HIAA remained unchanged, while the levels of dopamine metabolites, DOPAC and HVA, showed a significant decline. These results demonstrate evidence for a strong linkage between HFS in the STN and reduc- tion of the levels of serotonin in the caudate-putamen, which is likely responsible for psychiatric side effects seen in Park- insonian patients who are treated with STN stimulation.
{"title":"Modulation of Extracellular Levels of 5-HT in the Caudate Putamen of Freely Moving Rats by High Frequency Stimulation of the Subthalamic Nucleus","authors":"Kevin Joseph, R. Varatharajan, Sonya Neto, U. Hofmann, V. Tronnier, A. Moser","doi":"10.2174/1874082001408010014","DOIUrl":"https://doi.org/10.2174/1874082001408010014","url":null,"abstract":"Electrical high frequency stimulation (HFS) in the subthalamic nucleus (STN) has been shown to have a thera- peutic effect in several movement disorders. But, debilitating psychiatric effects like depression and suicidality are occa- sionally seen and might be caused by the changes in the serotoninergic activity. Previous studies could show that HFS of the STN results in inhibition of the serotonergic neurons originating in the dorsal raphe nucleus. The aim of this study was to characterize the effect of HFS (124 Hz, 0.5 mA) in the STN, on the extracellular levels of serotonin, dopamine and their metabolites HIAA, DOPAC and HVA in the caudate-putamen (CPu) in conscious and freely moving rats. Extracellular levels of the neurotransmitters and their metabolites were quantified using high performance liquid chromatography with electrochemical detection. Under HFS conditions, a significant reduction in the extracellular levels of serotonin was ob- served. Cessation of HFS showed a recovery back to basal levels. Dopamine levels were not affected, although significant increase of its metabolites DOPAC and HVA were measured. In the case of low frequency stimulation (LFS), levels of se- rotonin and its metabolite HIAA remained unchanged, while the levels of dopamine metabolites, DOPAC and HVA, showed a significant decline. These results demonstrate evidence for a strong linkage between HFS in the STN and reduc- tion of the levels of serotonin in the caudate-putamen, which is likely responsible for psychiatric side effects seen in Park- insonian patients who are treated with STN stimulation.","PeriodicalId":88753,"journal":{"name":"The open neuroscience journal","volume":"106 1","pages":"14-20"},"PeriodicalIF":0.0,"publicationDate":"2015-01-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"77883649","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}
Pub Date : 2014-04-18DOI: 10.2174/1874082001408010009
E. Polychronopoulos, P. Albrecht, Julia Tafazzoli-Lari, H. Iven, A. Moser
Objective: In this prospective study, we examined the association between azathioprine dose, levels of its phosphoribosylated metabolites, and the activity of thiopurine methyltransferase in patients with multiple sclerosis (MS). Materials/Methods: Clinical data and blood samples were collected from 27 MS patients who were undergoing azathio- prine treatment. In red blood cells, thiopurine methyltransferase (TPMT) activity was determined, and after hydrolysis and cleavage of the phosphoribosyl residue, amounts of 6-thioguanine (6-TG), 6-methyl-thioguanine (6-MTG), 6- methylmercaptopurine (6-MMP) were measured. For clinical evaluation, the expanded disability status score (EDSS) and the multiple sclerosis functional composite (MSFC) were performed. Laboratory and clinical examinations were con- ducted twice with a 6-month-intervall. Results: Over a broad range of daily azathioprine dose, nearly constant levels of the immunosuppressive-active 6-TG (nucleotides) were found. There was, however, a marked relationship between daily azathioprine dose and 6-MMP nucleotide levels. Especially patients receiving an azathioprine dose of more than 1.5 mg/kg per day in particular presented an exponential increase in 6-MMP levels when TPMT activity was higher than 45 U/g Hb. All the biochemical measurements gave similar results when performed 6 months later. Conclusions: Patients with the combination of a high TPMT-activity and an azathioprine dose of more than 1.5 mg/kg/d exhibit significantly in- creased 6-MMP nucleotide levels. These patients are thus at risk for hepatotoxic side effects. Determination of TPMT ac- tivity before azathioprine therapy and monitoring of its metabolites might provide guidance for dose individualization.
{"title":"Azathioprine Therapy in Multiple Sclerosis: Phosphoribosylated Metabolites and Thiopurine Methyltransferase Activity","authors":"E. Polychronopoulos, P. Albrecht, Julia Tafazzoli-Lari, H. Iven, A. Moser","doi":"10.2174/1874082001408010009","DOIUrl":"https://doi.org/10.2174/1874082001408010009","url":null,"abstract":"Objective: In this prospective study, we examined the association between azathioprine dose, levels of its phosphoribosylated metabolites, and the activity of thiopurine methyltransferase in patients with multiple sclerosis (MS). Materials/Methods: Clinical data and blood samples were collected from 27 MS patients who were undergoing azathio- prine treatment. In red blood cells, thiopurine methyltransferase (TPMT) activity was determined, and after hydrolysis and cleavage of the phosphoribosyl residue, amounts of 6-thioguanine (6-TG), 6-methyl-thioguanine (6-MTG), 6- methylmercaptopurine (6-MMP) were measured. For clinical evaluation, the expanded disability status score (EDSS) and the multiple sclerosis functional composite (MSFC) were performed. Laboratory and clinical examinations were con- ducted twice with a 6-month-intervall. Results: Over a broad range of daily azathioprine dose, nearly constant levels of the immunosuppressive-active 6-TG (nucleotides) were found. There was, however, a marked relationship between daily azathioprine dose and 6-MMP nucleotide levels. Especially patients receiving an azathioprine dose of more than 1.5 mg/kg per day in particular presented an exponential increase in 6-MMP levels when TPMT activity was higher than 45 U/g Hb. All the biochemical measurements gave similar results when performed 6 months later. Conclusions: Patients with the combination of a high TPMT-activity and an azathioprine dose of more than 1.5 mg/kg/d exhibit significantly in- creased 6-MMP nucleotide levels. These patients are thus at risk for hepatotoxic side effects. Determination of TPMT ac- tivity before azathioprine therapy and monitoring of its metabolites might provide guidance for dose individualization.","PeriodicalId":88753,"journal":{"name":"The open neuroscience journal","volume":"284 1","pages":"9-13"},"PeriodicalIF":0.0,"publicationDate":"2014-04-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"80231751","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}
Pub Date : 2014-02-07DOI: 10.2174/1874082001408010001
M. Kasai, Shoko Hososhima, Yun-Fei Liang
To determine whether fishes respond to menthol, Japanese medaka Oryzias latipes, goldfish Carassius auratus, and zebrafish Danio rerio were exposed to various types of menthol receptors agonists and the behavioral responses to these drugs were observed. Waterbone application of dl-menthol (0.5 mM) induced surgical anesthesia in 100% of medaka, 90% of goldfish, and 100% of zebrafish. The percentage of response increased dose-dependently from 0.2 mM to 0.5 mM. There were no differences in either percentage or latency of the response in surgical anesthesia among dl-, d-, and l- types of menthol. A high (3.0 mM) concentration of any of the three types of menthol induced rapid movement fol- lowed by the anesthetic response. Rapid movement was observed with allyl isothiocyanate, a cold nociceptor agonist, but not with icilin, a cold receptor agonist, in medaka and goldfish. Both allyl isothiocyanate and icilin failed to induce surgi- cal anesthesia. To determine the involvement of � -aminobutyric acid (GABA) system in menthol-induced surgical anes- thesia, the effect of the receptors antagonist for the GABAA was tested. Pretreatment with a specific GABAA receptor an- tagonist prolonged the latency of the anesthetic response to menthol, but not to cold-water stimulation, in medaka and goldfish. These results demonstrate that menthol can play a role in the induction of surgical anesthesia in fishes, related at least in part to the activation of GABAA receptors, and of rapid movement possibly via cold nociceptors.
{"title":"Menthol Induces Surgical Anesthesia and Rapid Movement in Fishes","authors":"M. Kasai, Shoko Hososhima, Yun-Fei Liang","doi":"10.2174/1874082001408010001","DOIUrl":"https://doi.org/10.2174/1874082001408010001","url":null,"abstract":"To determine whether fishes respond to menthol, Japanese medaka Oryzias latipes, goldfish Carassius auratus, and zebrafish Danio rerio were exposed to various types of menthol receptors agonists and the behavioral responses to these drugs were observed. Waterbone application of dl-menthol (0.5 mM) induced surgical anesthesia in 100% of medaka, 90% of goldfish, and 100% of zebrafish. The percentage of response increased dose-dependently from 0.2 mM to 0.5 mM. There were no differences in either percentage or latency of the response in surgical anesthesia among dl-, d-, and l- types of menthol. A high (3.0 mM) concentration of any of the three types of menthol induced rapid movement fol- lowed by the anesthetic response. Rapid movement was observed with allyl isothiocyanate, a cold nociceptor agonist, but not with icilin, a cold receptor agonist, in medaka and goldfish. Both allyl isothiocyanate and icilin failed to induce surgi- cal anesthesia. To determine the involvement of � -aminobutyric acid (GABA) system in menthol-induced surgical anes- thesia, the effect of the receptors antagonist for the GABAA was tested. Pretreatment with a specific GABAA receptor an- tagonist prolonged the latency of the anesthetic response to menthol, but not to cold-water stimulation, in medaka and goldfish. These results demonstrate that menthol can play a role in the induction of surgical anesthesia in fishes, related at least in part to the activation of GABAA receptors, and of rapid movement possibly via cold nociceptors.","PeriodicalId":88753,"journal":{"name":"The open neuroscience journal","volume":"47 1","pages":"1-8"},"PeriodicalIF":0.0,"publicationDate":"2014-02-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"88266266","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}
Pub Date : 2013-10-18DOI: 10.2174/1874082001307010005
Nicholas A. Altieri
This study investigated the extent to which audiovisual speech integration is special by comparing behavioral and neural measures using both speech and non-speech stimuli. An audiovisual recognition experiment presenting listen- ers with auditory, visual, and audiovisual stimuli was implemented. The auditory component consisted of sine wave speech, and the visual component consisted of point light displays, which include point-light dots that highlight a talker's points of articulation. In the first phase, listeners engaged in a discrimination task where they were unaware of the linguis- tic nature of the auditory and visual stimuli. In the second phase, they were informed that the auditory and visual stimuli were spoken utterances of /be/ ("bay") and /de/ ("day"), and they engaged in the same task. The neural dynamics of audiovisual integration was investigated by utilizing EEG, including mean Global Field Power and current density recon- struction (CDR). As predicted, support for divergent regions of multisensory integration between the speech and non- speech stimuli was obtained, namely greater posterior parietal activation in the non-speech condition. Conversely, reac- tion-time measures indicated qualitatively similar multisensory integration across experimental conditions.
{"title":"Neural Dynamics of Audiovisual Integration for Speech and Non-Speech Stimuli: A Psychophysical Study","authors":"Nicholas A. Altieri","doi":"10.2174/1874082001307010005","DOIUrl":"https://doi.org/10.2174/1874082001307010005","url":null,"abstract":"This study investigated the extent to which audiovisual speech integration is special by comparing behavioral and neural measures using both speech and non-speech stimuli. An audiovisual recognition experiment presenting listen- ers with auditory, visual, and audiovisual stimuli was implemented. The auditory component consisted of sine wave speech, and the visual component consisted of point light displays, which include point-light dots that highlight a talker's points of articulation. In the first phase, listeners engaged in a discrimination task where they were unaware of the linguis- tic nature of the auditory and visual stimuli. In the second phase, they were informed that the auditory and visual stimuli were spoken utterances of /be/ (\"bay\") and /de/ (\"day\"), and they engaged in the same task. The neural dynamics of audiovisual integration was investigated by utilizing EEG, including mean Global Field Power and current density recon- struction (CDR). As predicted, support for divergent regions of multisensory integration between the speech and non- speech stimuli was obtained, namely greater posterior parietal activation in the non-speech condition. Conversely, reac- tion-time measures indicated qualitatively similar multisensory integration across experimental conditions.","PeriodicalId":88753,"journal":{"name":"The open neuroscience journal","volume":"97 3 1","pages":"5-18"},"PeriodicalIF":0.0,"publicationDate":"2013-10-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"84715303","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}
Sensory epithelial cells in the organ of Corti survive throughout life. However, factors for sensory epithelial cell survival are poorly understood at the present time. Here we demonstrated that brain-derived neurotrophic factor (BDNF), a factor committing to neuronal survival, promotes the survival of sensory epithelial cells (OC1) through phos- phatidylinositide 3'-OH kinase (PI3K)/protein kinase B (Akt) and/or nuclear factor kappa B (NF- B)/B cell lymphoma 2 (Bcl-2) pathways. BDNF activated PI3K/Akt kinases and increased NF-B/Bcl-2 activity or expression in association with the survival of OC1 cells in vitro. LY294002, a specific inhibitor for PI3K, and pyrrolidine dithiocarbamate (PDTC), an inhibitor for NF-B, abrogated the protective effect of BDNF on OC1 cells, causing the increased expression of caspase 3 and the apoptotic cell numbers in vitro. Similarly, a dominant negative mutant of I kappa B alpha (I BM, a specific inhibitor of NF-B) abrogated the protective effect of BDNF on OC1 cells. The data demonstrate that BDNF promotes the survival of sensory epithelial cells through the PI3K/Akt and NF- B/Bcl-2 signaling pathways.
Corti器官中的感觉上皮细胞终生存活。然而，目前对感觉上皮细胞存活的因素了解甚少。在这里，我们证明脑源性神经营养因子(BDNF)，一个参与神经元存活的因子，通过phos- phatidylinositide 3'- oh激酶(PI3K)/蛋白激酶B (Akt)和/或核因子κ B (NF-B)/B细胞淋巴瘤2 (Bcl-2)途径促进感觉上皮细胞(OC1)的存活。BDNF激活PI3K/Akt激酶，增加NF-B/Bcl-2活性或表达，与OC1细胞体外存活相关。PI3K特异性抑制剂LY294002和NF-B抑制剂pyrrolidine dithiocarbamate (PDTC)使BDNF对OC1细胞的保护作用失效，导致体外caspase 3表达增加，凋亡细胞数量增加。同样，I kappa B α的显性负突变体(IBM, NF-B的特异性抑制剂)取消了BDNF对OC1细胞的保护作用。数据表明，BDNF通过PI3K/Akt和NF-B/Bcl-2信号通路促进感觉上皮细胞的存活。
{"title":"BDNF promotes the survival of rat sensory epithelial cells via the PI3K/Akt and NF-κB/Bcl-2 signaling pathways","authors":"Jianmin Huang, Xiaohua Hu, Ling Feng, Shinji Fukudome, Yiqing Zheng, Jizhen Lin","doi":"10.2174/1874082001307010019","DOIUrl":"https://doi.org/10.2174/1874082001307010019","url":null,"abstract":"Sensory epithelial cells in the organ of Corti survive throughout life. However, factors for sensory epithelial cell survival are poorly understood at the present time. Here we demonstrated that brain-derived neurotrophic factor (BDNF), a factor committing to neuronal survival, promotes the survival of sensory epithelial cells (OC1) through phos- phatidylinositide 3'-OH kinase (PI3K)/protein kinase B (Akt) and/or nuclear factor kappa B (NF- B)/B cell lymphoma 2 (Bcl-2) pathways. BDNF activated PI3K/Akt kinases and increased NF-B/Bcl-2 activity or expression in association with the survival of OC1 cells in vitro. LY294002, a specific inhibitor for PI3K, and pyrrolidine dithiocarbamate (PDTC), an inhibitor for NF-B, abrogated the protective effect of BDNF on OC1 cells, causing the increased expression of caspase 3 and the apoptotic cell numbers in vitro. Similarly, a dominant negative mutant of I kappa B alpha (I BM, a specific inhibitor of NF-B) abrogated the protective effect of BDNF on OC1 cells. The data demonstrate that BDNF promotes the survival of sensory epithelial cells through the PI3K/Akt and NF- B/Bcl-2 signaling pathways.","PeriodicalId":88753,"journal":{"name":"The open neuroscience journal","volume":"27 2 1","pages":"19-27"},"PeriodicalIF":0.0,"publicationDate":"2013-10-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"77382619","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}
Pub Date : 2013-09-20DOI: 10.2174/1874082020130807001
Nanette Messemer, Christin Kunert, P. Illés, P. Rubini
Co-localization of P2X4 and P2X7 subunits has been demonstrated in a number of tissues. It appears that these subunits form functionally interacting homomeric P2X4 and P2X7 receptors rather than heteromeric P2X4/7 receptors. We have recently reported that adult neural progenitor cells (NPCs) of the mouse subventricular zone (SVZ) possess P2X7 receptors. Cultured proliferating NPCs responded to higher concentrations of the prototypic P2X7 agonist diben- zoyl-ATP (Bz-ATP) with inward current, strongly inhibited by the selective P2X7 antagonist A438079, and moderately depressed by the P2X1-3,4 antagonist TNP-ATP, or the selective P2X4 antagonist 5-BDBD. Now we show in addition that ivermectin, a selective allosteric modulator of P2X4 receptors, uniformly potentiated the effect of lower Bz-ATP con- centrations; this potentiation was abolished by 5-BDBD. In conclusion, astrocyte-like cultured SVZ NPCs are endowed with P2X4 and P2X7 receptors shaping the characteristics of these cells with respect to ATP-dependent signalling.
{"title":"Co-expression of functional P2X4 and P2X7 receptors at adult neural progenitor cells of the mouse subventricular zone","authors":"Nanette Messemer, Christin Kunert, P. Illés, P. Rubini","doi":"10.2174/1874082020130807001","DOIUrl":"https://doi.org/10.2174/1874082020130807001","url":null,"abstract":"Co-localization of P2X4 and P2X7 subunits has been demonstrated in a number of tissues. It appears that these subunits form functionally interacting homomeric P2X4 and P2X7 receptors rather than heteromeric P2X4/7 receptors. We have recently reported that adult neural progenitor cells (NPCs) of the mouse subventricular zone (SVZ) possess P2X7 receptors. Cultured proliferating NPCs responded to higher concentrations of the prototypic P2X7 agonist diben- zoyl-ATP (Bz-ATP) with inward current, strongly inhibited by the selective P2X7 antagonist A438079, and moderately depressed by the P2X1-3,4 antagonist TNP-ATP, or the selective P2X4 antagonist 5-BDBD. Now we show in addition that ivermectin, a selective allosteric modulator of P2X4 receptors, uniformly potentiated the effect of lower Bz-ATP con- centrations; this potentiation was abolished by 5-BDBD. In conclusion, astrocyte-like cultured SVZ NPCs are endowed with P2X4 and P2X7 receptors shaping the characteristics of these cells with respect to ATP-dependent signalling.","PeriodicalId":88753,"journal":{"name":"The open neuroscience journal","volume":"18 1","pages":"1-4"},"PeriodicalIF":0.0,"publicationDate":"2013-09-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"84718966","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}
Pub Date : 2012-03-30DOI: 10.2174/1874082001206010010
A. Hiura, H. Nakagawa
Studies into the interactions between glia/immune cells and neurons have focused on the induction of patho-logical (neuropathic or inflammatory) pain. Growing evidence of close relationships between peripheral and central glia and pathological pain has emerged during the last 2 decades. Numerous experimental studies have showed the release of cytokines and inflammatory neuropeptides from peripheral and central terminals of primary sensory neurons and from ac-tivated peripheral and central glia after nerve injury (crush, ligation or transection), which in turn act in a paracrine or autocrine manner. Cytokines induce the synthesis of algogens (pain-inducing substances such as prostaglandin) which leads to the primary (peripheral) or secondary (central) sensitization responsible for hyperalgesia or allodynia under in-flammatory conditions. The review has also highlighted the role of thermo transient receptor potential (TRP) channels TRPV1, TRPA1 and TRPM8 in the induction of pathological pain. The noxious heat sensor TRPV1 has an overt role in noxious heat hyperalgesia or allodynia, whereas TRPA1 and TRPM8 seem to have roles in noxious cold or mechanical al-lodynia, although results are inconsistent. Close mutual interrelationships between immune and glial cells and thermoTRP channels via cytokines or pro-inflammatory neuropeptides cannot be ignored when attempting to explain the induction and continuation of pathological pain. Investigations on the initial signals sent to the central area (superficial dorsal horn) remote from injured (or infectious) sites are a key point to clarify the mechanisms of pathological pain.
{"title":"Roles of Glia, Immune Cells and the Thermo-TRP Channels, TRPV1, TRPA1 and TRPM8, in Pathological Pain","authors":"A. Hiura, H. Nakagawa","doi":"10.2174/1874082001206010010","DOIUrl":"https://doi.org/10.2174/1874082001206010010","url":null,"abstract":"Studies into the interactions between glia/immune cells and neurons have focused on the induction of patho-logical (neuropathic or inflammatory) pain. Growing evidence of close relationships between peripheral and central glia and pathological pain has emerged during the last 2 decades. Numerous experimental studies have showed the release of cytokines and inflammatory neuropeptides from peripheral and central terminals of primary sensory neurons and from ac-tivated peripheral and central glia after nerve injury (crush, ligation or transection), which in turn act in a paracrine or autocrine manner. Cytokines induce the synthesis of algogens (pain-inducing substances such as prostaglandin) which leads to the primary (peripheral) or secondary (central) sensitization responsible for hyperalgesia or allodynia under in-flammatory conditions. The review has also highlighted the role of thermo transient receptor potential (TRP) channels TRPV1, TRPA1 and TRPM8 in the induction of pathological pain. The noxious heat sensor TRPV1 has an overt role in noxious heat hyperalgesia or allodynia, whereas TRPA1 and TRPM8 seem to have roles in noxious cold or mechanical al-lodynia, although results are inconsistent. Close mutual interrelationships between immune and glial cells and thermoTRP channels via cytokines or pro-inflammatory neuropeptides cannot be ignored when attempting to explain the induction and continuation of pathological pain. Investigations on the initial signals sent to the central area (superficial dorsal horn) remote from injured (or infectious) sites are a key point to clarify the mechanisms of pathological pain.","PeriodicalId":88753,"journal":{"name":"The open neuroscience journal","volume":"96 1","pages":"10-26"},"PeriodicalIF":0.0,"publicationDate":"2012-03-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"85860303","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}
Pub Date : 2012-01-19DOI: 10.2174/1874082001206010001
A. Herbert
We describe a simple Hadamard design for neural architecture with an equal number of input and output ele- ments that is both error-tolerant and robust to missing information. The design provides a basis for calculation using a classification scheme based on the Chinese remainder theorem, producing an abstract representation of the physical world. The underlying co-prime arrays can be generated in a simple manner biologically and can evolve into more complex de- signs. The approach differs from previously described neural network constructions in that all connectivity is specified by design, with each correctly wired array producing a single output for each subset of inputs. The wiring is consistent with the "On-Off" schema observed for different senses because only about half the inputs can be active at any one time. The arrays can be tuned through by varying the number of simultaneous inputs required for activation within a range specified by the array size. The architecture is scalable.
{"title":"A Neural Architecture Based on Hadamard Designs","authors":"A. Herbert","doi":"10.2174/1874082001206010001","DOIUrl":"https://doi.org/10.2174/1874082001206010001","url":null,"abstract":"We describe a simple Hadamard design for neural architecture with an equal number of input and output ele- ments that is both error-tolerant and robust to missing information. The design provides a basis for calculation using a classification scheme based on the Chinese remainder theorem, producing an abstract representation of the physical world. The underlying co-prime arrays can be generated in a simple manner biologically and can evolve into more complex de- signs. The approach differs from previously described neural network constructions in that all connectivity is specified by design, with each correctly wired array producing a single output for each subset of inputs. The wiring is consistent with the \"On-Off\" schema observed for different senses because only about half the inputs can be active at any one time. The arrays can be tuned through by varying the number of simultaneous inputs required for activation within a range specified by the array size. The architecture is scalable.","PeriodicalId":88753,"journal":{"name":"The open neuroscience journal","volume":"1 1","pages":"1-9"},"PeriodicalIF":0.0,"publicationDate":"2012-01-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"90810730","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}
Pub Date : 2011-08-02DOI: 10.2174/1874082001105010024
M. Rostami, S. M. Hosseini, M. Takahashi, M. Sugiura, R. Kawashima
In recent years, the neural substrates underlying outcome feedback processing have been investigated in several neuroimaging studies of feedback-based learning. However, what has been missed in these studies is that, the learning process itself also affects the way the feedback is being processed. In this study, we tried to investigate the changes in neural substrates underlying positive and negative feedback processing during goal-directed implicit learning using the Sugar Production Factory (SPF) task in conjunction with an event related functional magnetic resonance imaging. We found a significant learning-related decrease in activity of the right superior frontal gyrus (SFG) in response to positive feedback and a learning-related increase in activity of the precuneus in response to negative feedback. The results demon- strate the changing role of feedback during learning and suggest that learning-related changes in activity of the SFG and precuneus that have been previously reported in several implicit learning studies arise from changes in feedback process- ing after learning. In addition, the results suggest the important role of positive feedback in early stage and negative feed- back in late stage of goal-directed implicit learning.
{"title":"Changes in Neural Correlates of Outcome Feedback Processing During Implicit Learning","authors":"M. Rostami, S. M. Hosseini, M. Takahashi, M. Sugiura, R. Kawashima","doi":"10.2174/1874082001105010024","DOIUrl":"https://doi.org/10.2174/1874082001105010024","url":null,"abstract":"In recent years, the neural substrates underlying outcome feedback processing have been investigated in several neuroimaging studies of feedback-based learning. However, what has been missed in these studies is that, the learning process itself also affects the way the feedback is being processed. In this study, we tried to investigate the changes in neural substrates underlying positive and negative feedback processing during goal-directed implicit learning using the Sugar Production Factory (SPF) task in conjunction with an event related functional magnetic resonance imaging. We found a significant learning-related decrease in activity of the right superior frontal gyrus (SFG) in response to positive feedback and a learning-related increase in activity of the precuneus in response to negative feedback. The results demon- strate the changing role of feedback during learning and suggest that learning-related changes in activity of the SFG and precuneus that have been previously reported in several implicit learning studies arise from changes in feedback process- ing after learning. In addition, the results suggest the important role of positive feedback in early stage and negative feed- back in late stage of goal-directed implicit learning.","PeriodicalId":88753,"journal":{"name":"The open neuroscience journal","volume":"3 1","pages":"24-30"},"PeriodicalIF":0.0,"publicationDate":"2011-08-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"75244806","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}
Pub Date : 2011-05-13DOI: 10.2174/1874082001105010016
R. Guex, F. Cerić, E. Hurtado, R. González, Alvaro Navarro, F. Manes, A. Ibanez
The goal of this study is to assess the role of membership and valence effects on errors performed in a racial implicit association test indexed by event-related potentials (ERPs). Non-indigenous participants performed an implicit association test (IAT) paradigm emphasizing the feedback of error due to misclassification of ingroup (non-indigenous) and outgroup (indigenous) faces as well as positive and negative words. As expected, participants responded to the com- patible task with higher accuracy than to incompatible tasks. This is the first report demonstrating that IAT errors produce electrophysiological ERP modulation. Our results suggest that medial frontal negativity is modulated not only by IAT er- ror of membership and valence classifications but also by IAT compatible and incompatible tasks. These results provide a basis for the future use of the misclassification error in the IAT recorded simultaneously with ERPs in other classic social psychology contexts.
{"title":"Performance Errors of in Group/ Out Group Stimuli and Valence Association in the Implicit Association Test: Brain Bias of Ingroup Favoritism","authors":"R. Guex, F. Cerić, E. Hurtado, R. González, Alvaro Navarro, F. Manes, A. Ibanez","doi":"10.2174/1874082001105010016","DOIUrl":"https://doi.org/10.2174/1874082001105010016","url":null,"abstract":"The goal of this study is to assess the role of membership and valence effects on errors performed in a racial implicit association test indexed by event-related potentials (ERPs). Non-indigenous participants performed an implicit association test (IAT) paradigm emphasizing the feedback of error due to misclassification of ingroup (non-indigenous) and outgroup (indigenous) faces as well as positive and negative words. As expected, participants responded to the com- patible task with higher accuracy than to incompatible tasks. This is the first report demonstrating that IAT errors produce electrophysiological ERP modulation. Our results suggest that medial frontal negativity is modulated not only by IAT er- ror of membership and valence classifications but also by IAT compatible and incompatible tasks. These results provide a basis for the future use of the misclassification error in the IAT recorded simultaneously with ERPs in other classic social psychology contexts.","PeriodicalId":88753,"journal":{"name":"The open neuroscience journal","volume":"140 1","pages":"16-23"},"PeriodicalIF":0.0,"publicationDate":"2011-05-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"78871516","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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