M. Reiner, Maria Stylianou-Korsnes, G. Glover, K. Hugdahl, Marcus W. Feldman
{"title":"Seeing Shapes and Hearing Textures: Two Neural Categories of Touch","authors":"M. Reiner, Maria Stylianou-Korsnes, G. Glover, K. Hugdahl, Marcus W. Feldman","doi":"10.2174/1874082001105010008","DOIUrl":"https://doi.org/10.2174/1874082001105010008","url":null,"abstract":"Touching for shape recognition has been shown to activate occipital areas in addition to somatosensory areas. In this study we asked if this combination of somatosensory and other sensory processing areas also exist in other kinds of touch recognition. In particular, does touch for texture roughness matching activate other sensory processing areas apart from somatosensory areas? We addressed this question with functional magnetic resonance imaging (fMRI) using wooden abstract stimulus objects whose shape or texture were to be identified. The participants judged if pairs of objects had the same shape or the same texture. We found that the activated brain areas for texture and shape matching have similar underlying structures, a combination of the primary motor area and somatosensory areas. Areas associated with object-shape processing were activated between stimuli during shape matching and not texture roughness matching, while auditory areas were activated during encoding of texture and not for shape stimuli. Matching of textures also in- volves left BA47, an area associated with retrieval of relational information. We suggest that texture roughness is recog- nized in a framework of ordering. Left-lateralized activations favoring texture might reflect semantic processing associ- ated with grading roughness quantitatively, as opposed to the more qualitative distinctions between shapes.","PeriodicalId":88753,"journal":{"name":"The open neuroscience journal","volume":"7 1","pages":"8-15"},"PeriodicalIF":0.0,"publicationDate":"2011-04-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"72993509","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
M. Haile, P. Broderick, Yong-sheng Li, T. Blanck, D. Quartermain, A. Bekker
{"title":"Nimodipine Reverses the Elevation of Synaptic Striatal Dopamine and Serotonin During In Vivo Hypoxia","authors":"M. Haile, P. Broderick, Yong-sheng Li, T. Blanck, D. Quartermain, A. Bekker","doi":"10.2174/1874082001105010001","DOIUrl":"https://doi.org/10.2174/1874082001105010001","url":null,"abstract":"Introduction: Moderate hypoxia has been implicated in the development of delirium. One mechanism may be an increase of Dopamine (DA) and Serotonin (5-HT) levels. Our previous studies indicated that hypoxia increased levels of both neurotransmitters (NT) and that nimodipine (NIMO) administered immediately after hypoxia preserved short term memory. We tested the hypothesis that these observations may be related to a NIMO dependent reduction of hypoxia in- duced NT elevation. Methods: Following IACUC approval, In Vivo microvoltammetry sensors (BRODERICK PROBE ® ) were implanted in the dorsal striatum of Na Pentobarbital anesthetized adult Sprague-Dawley rats. Extracellular NT levels were recorded for 15m during the establishment of baseline values in room air (N=6). Three sequential thirty-minute periods under hypoxia (10% O2) followed. First: under hypoxia alone; second after i.p. injection of NIMO (0.1mg/kg); and third following i.p. injection of NIMO (1.0mg/kg). Measurements were analyzed with ANOVA with post hoc Tukeys test. P-values less than 0.05 were considered significant. Results: NT levels are expressed as percentages of baseline values. Treatment values were averaged over each sequential thirty-minute period following each intervention. Moderate hypoxia resulted in the increase of DA to 172% (SEM=18) and 5-HT to 68% (SEM=4) above baseline. Under continuing hypoxia, NIMO (0.1mg/kg) caused DA levels to fall to 112% (SEM=14) and 5-HT to 13% (SEM=5) above baseline. NIMO (1.0mg/kg) caused DA levels to fall to 34% (SEM=6) above baseline and 5-HT to 20% (SEM=2) below baseline. Conclusion: Moderate hypoxia increased levels of DA and 5-HT in the striatum of rats. NIMO administration during on- going hypoxia caused the levels of both neurotransmitters to fall towards baseline. The results may have implications for understanding and treating cognitive decline due to hypoxia.","PeriodicalId":88753,"journal":{"name":"The open neuroscience journal","volume":"86 1","pages":"1-7"},"PeriodicalIF":0.0,"publicationDate":"2011-03-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"83942441","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}
{"title":"The Modulation of Synaptic Transmission by the Glial Purinergic System","authors":"Kazuhide Inoue, F. Kato, M. Tsuda","doi":"10.2174/1874082001004010084","DOIUrl":"https://doi.org/10.2174/1874082001004010084","url":null,"abstract":"Abstract: Accumulating evidence indicates that bioactive substances produced by glia play an important role in the modulation of synaptic transmission. Astrocytes and microglia express many types of P2 purinoceptors and the stimula-tion of these receptors causes the release of bioactive substances, termed “gliotransmitters”, such as ATP, glutamate and cytokines. Gliotransmitters are able to modulate synaptic transmission. In this article, the P2X 4 R and P2Y 12 R systems of microglia, which modulate the synaptic transmission between dorsal root ganglion neurons and dorsal horn neurons, are described. In addition, the role of the astrocyte purinergic system in synaptic transmission is discussed. The modulation of synaptic transmission by glial purinergic systems is a novel perspective on the regulation of brain and nerve function and is a new target for the development of medicines. Keywords: ATP receptors, microglia, astrocyte, synaptic transmission. 1. INTRODUCTION In 1972, Burnstock proposed new a role for nucleotides; that of neurotransmission [1]. Recently, numerous subtypes of ATP and adenosine receptor have been cloned, which has led to the acceptance of the “purinergic nervous system”. Now purinergic receptors are divided into two big families, P1 (receptors for adenosine and AMP) and P2 (receptors for nucleotides). Four subtypes of P1 receptors have been cloned, namely, A","PeriodicalId":88753,"journal":{"name":"The open neuroscience journal","volume":"62 1","pages":"84-92"},"PeriodicalIF":0.0,"publicationDate":"2010-07-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"78693082","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}
{"title":"Purinergic Signalling in the CNS","authors":"G. Burnstock","doi":"10.2174/1874082001004010024","DOIUrl":"https://doi.org/10.2174/1874082001004010024","url":null,"abstract":"Purinergic neurotransmission, involving release of ATP as an efferent neurotransmitter was first proposed in 1972. Later it was recognised as a cotransmitter in peripheral nerves and more recently as a cotransmitter with glutamate, noradrenaline, GABA, acetylcholine and dopamine in the CNS. Both ion channel and G protein-coupled receptors for purines and pyrimidines are widely expressed in the brain and spinal cord. They mediate both fast signalling in neuro- transmission and neuromodulation and long-term (trophic) signalling in cell proliferation, differentiation and death. Purinergic signalling is prominent in neuron-glial cell interactions. Purinergic signalling has been implicated in learning and memory, locomotor activity and feeding behaviour. There is increasing interest in the involvement of purinergic sig- nalling in the pathophysiology of the CNS, including trauma, ischaemia, epilepsy, neurodegenerative diseases, neuropsy- chiatric and mood disorders.","PeriodicalId":88753,"journal":{"name":"The open neuroscience journal","volume":"129 1","pages":"24-30"},"PeriodicalIF":0.0,"publicationDate":"2010-07-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"90229814","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}
{"title":"Editorial: [Purinergic Signalling in Epilepsy]","authors":"D. Boison, G. Burnstock","doi":"10.2174/1874082001004010023","DOIUrl":"https://doi.org/10.2174/1874082001004010023","url":null,"abstract":"","PeriodicalId":88753,"journal":{"name":"The open neuroscience journal","volume":"5 1","pages":"23-23"},"PeriodicalIF":0.0,"publicationDate":"2010-07-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"81916830","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}
{"title":"Role of The Purinergic Neuromodulation System in Epilepsy","authors":"Â. R. Tomé, H. Silva, R. Cunha","doi":"10.2174/1874082001004010064","DOIUrl":"https://doi.org/10.2174/1874082001004010064","url":null,"abstract":"Adenosine has long been considered an endogenous anti-epileptic compound. This concept was based on the widespread distribution of adenosine A1 receptors (A1R), which are mostly located in excitatory synapses; here, A1R in- hibit glutamate release, decrease glutamatergic responsiveness and hyperpolarise neurons. However, the combined obser- vation that synaptic A1R undergo desensitisation in chronic noxious situations whereas the activation of A1R still prevents seizure activity suggests that the A1R anti-epileptic action may involve non-synaptic mechanisms. Two alternative mechanisms can be considered to explain the ability of A1R to control seizure activity and resulting neurodegeneration: 1) the possible role of A1R-mediated control of metabolism; 2) the A1R-mediated preconditioning involving a coordinated control of neuron-glia communication. However, purinergic modulation of seizure activity is likely to involve other sys- tems apart from A1R. Thus, the blockade of adenosine A2A receptors (A2AR), which density increases in animal models of epilepsy, can attenuate seizure activity and prevent seizure-induced neurodegeneration. Furthermore, ATP, which is the main source of the endogenous adenosine activating A2AR, also act as a general danger signal and may also directly con- trol seizure activity through P2 receptors (P2R). Therefore, the purinergic control of epilepsy may actually involve differ- ent parallel signalling arms, some beneficial and others deleterious, probably acting at different sites (in epileptic foci and in their neighbourhood) and at different times. It is likely that combined targeting of different purinergic receptors may be the most efficacious way to control seizure activity, its spreading and the resulting neurodegeneration.","PeriodicalId":88753,"journal":{"name":"The open neuroscience journal","volume":"6 1","pages":"64-83"},"PeriodicalIF":0.0,"publicationDate":"2010-07-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"74558677","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}
{"title":"Adenosine - A Physiological Regulator and a Distress Signal","authors":"B. Fredholm","doi":"10.2174/1874082001004010053","DOIUrl":"https://doi.org/10.2174/1874082001004010053","url":null,"abstract":"Abstract: The present brief review argues the case that adenosine can be both a distress signal and a physiological regula-tor. A key factor in determining which of these possibilities pertain is related to the number of receptors expressed. As the signaling from the adenosine receptor to the functional response generally involves amplification, we have a situation in-volving so called spare receptors. This has the consequence that alterations in the receptor number lead to shifts in the po-tency of the endogenous agonist rather than a shift in the maximum response elicited. The roles of adenosine are studied by antagonists and/or animals (mostly mice) with targeted deletions of receptors or enzymes involved in adenosine me-tabolism. Whereas, adaptive changes in the genetically modified mice can occur for the physiologically important effects, such adaptive changes are less likely to occur for the situations when adenosine acts as a distress signal. Keywords: Adenosine receptors, ATP, genetically modified mice, receptor reserve. There are four evolutionarily well conserved receptors for adenosine denoted A","PeriodicalId":88753,"journal":{"name":"The open neuroscience journal","volume":"66 1","pages":"53-57"},"PeriodicalIF":0.0,"publicationDate":"2010-07-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"90877334","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}
{"title":"The Role of the Guanine-Based Purinergic System in Seizures and Epilepsy","authors":"André Schmidt, D. Souza","doi":"10.2174/1874082001004010102","DOIUrl":"https://doi.org/10.2174/1874082001004010102","url":null,"abstract":"Guanine-based purines have been traditionally studied as modulators of intracellular processes, mainly G- protein activity. However, more recently, several studies have shown that they exert a variety of extracellular effects not related to G-proteins, including trophic effects on neural cells, modulation of glutamatergic activity, behavioral effects and anticonvulsant activity. In this article, the putative effects of the guanine-based purines against seizures and neurotox- icity are reviewed. Current evidence suggests that guanine-based purines, especially guanosine, seem to be endogenous anticonvulsant substances, perhaps in a similar way to the adenine-based purines. Although studies addressing the mecha- nism of action of guanine-based purines are still lacking, their anticonvulsant activity is probably related to the modula- tion of several glutamatergic parameters, especially the astrocytic glutamate uptake. These findings point to the guanine- based purines as potential new targets for the development of novel drugs for neuroprotection and management of epi- lepsy.","PeriodicalId":88753,"journal":{"name":"The open neuroscience journal","volume":"97 1","pages":"102-113"},"PeriodicalIF":0.0,"publicationDate":"2010-07-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"88971682","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}
{"title":"Ectonucleotidases and Epilepsy","authors":"G. P. Cognato, C. Bonan","doi":"10.2174/1874082001004010044","DOIUrl":"https://doi.org/10.2174/1874082001004010044","url":null,"abstract":"Adenosine has been proposed as an endogenous anticonvulsant which can play an important role in seizure ini- tiation, propagation and arrest. Extracellular ATP and adenosine are able to modulate synaptic activity through activation of P2 (P2X and P2Y) and P1 receptors (A1, A2A, A2B, and A3), respectively. Besides the release of adenosine per se, the levels of ATP and adenosine in the synaptic cleft are controlled by a complex cascade of cell surface-localized enzymes collectively known as ectonucleotidases. These enzymes are capable of hydrolyzing nucleoside triphosphates, diphos- phates and monophosphates to their respective nucleosides. There are four major families of ectonucleotidases: ecto- nucleoside triphosphate diphosphohydrolases (E-NTPDases), ecto-nucleotide pyrophosphatase/phosphodiesterases (E- NPPs), alkaline phosphatases and ecto-5'-nucleotidase. All these members have specific physiological functions in the brain. In this review, the involvement of ectonucleotidases in the pathophysiology of brain disorders, such as seizures and epilepsy, is discussed. A brief introduction about the general characteristics of these enzymes is followed by a discussion about the role of ectonucleotidases in epilepsy and seizures and the implications for future treatments.","PeriodicalId":88753,"journal":{"name":"The open neuroscience journal","volume":"6 1","pages":"44-52"},"PeriodicalIF":0.0,"publicationDate":"2010-07-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"76379901","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}
{"title":"Pathophysiological Aspects of Temporal Lobe Epilepsy and the Role of P2X Receptors","authors":"M. Fernandes, M. G. Mazzacoratti, E. Cavalheiro","doi":"10.2174/1874082001004010035","DOIUrl":"https://doi.org/10.2174/1874082001004010035","url":null,"abstract":"In the central nervous system (CNS), ATP is released from vesicles at nerve terminals in a frequency- dependent manner and can activate P2 receptors widely expressed and distributed in the CNS. In addition to interacting with P2 receptors, ATP can be rapidly hydrolyzed to adenosine to activate P1 receptors modulating neuronal transmission. Thus, complex synaptic interactions in the CNS are modulated by P2 and P1 receptors. This review focuses on the role of P2X receptors in temporal lobe epilepsy. P2X receptors are cationic-selective channels gated by extracellular ATP. Seven subunits (P2X1-7) are expressed throughout the central nervous system and are involved with modulatory mechanisms of neurotransmitter release, hyperexcitability, intracellular calcium influx, cell-cell communication, neuroprotection, and cell death. This review discusses the current data regarding the involvement of P2 receptors in the pathophysiology of tempo- ral lobe epilepsy (TLE).","PeriodicalId":88753,"journal":{"name":"The open neuroscience journal","volume":"1 1","pages":"35-43"},"PeriodicalIF":0.0,"publicationDate":"2010-07-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"90873494","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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