The open neuroscience journal最新文献

{"title":"Editorial: Exciting Dendritic Spines","authors":"Chi W. Pak, J. R. Bamburg","doi":"10.2174/1874082000903020052","DOIUrl":"https://doi.org/10.2174/1874082000903020052","url":null,"abstract":"The ability of a synapse to alter its strength based on use (synaptic plasticity) reigns as the basis of most cellular models of learning and memory [1]. However, if synaptic plasticity is king, then the dendritic spine is its kingdom. The dendritic spine, which houses the majority of excitatory synapses in the mammalian central nervous system, also undergoes dynamic changes to its shape (structural plasticity) in an activity-dependent manner. Indeed, strengthening of the synapse, or long-term potentiation (LTP), is often associated with spine head enlargement, whereas weakening of the synapse, or long-term depression (LTD), is often associated with spine head shrinkage. Underlying structural plasticity is the cytoskeleton protein, actin, whose dynamics and organization ultimately shape spine morphology, and which can also influence synaptic plasticity through modulation of membrane receptor insertion, removal and function. Thus, actin is both governed by and governs the king and kingdom. This special issue of The Open Neuroscience Journal explores many different aspects of dendritic spine morphology, regulation and function in health and disease.","PeriodicalId":88753,"journal":{"name":"The open neuroscience journal","volume":"179 1","pages":"52-53"},"PeriodicalIF":0.0,"publicationDate":"2009-11-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"85047673","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 Production and Degradation of Serotonin During Development","authors":"K. Nakamura, H. Hasegawa","doi":"10.2174/1874082000903010035","DOIUrl":"https://doi.org/10.2174/1874082000903010035","url":null,"abstract":"Serotonin (5-hydroxytryptamine (5-HT)) is one of the major neurotransmitter in the brain. Since 5-HT is car- ried by 5-HT transporters and the biological activities of 5-HT are exerted through 5-HT receptors, disturbed regulation of 5-HT transporters and receptors in the adult brain has been implicated in pathological conditions in central nervous sys- tems. On the other hand, proper 5-HT neurotransmission during development underlies the mature functional architecture of serotonergic neurons, and an increasing body of evidence suggests the involvement of developmental brain distur- bances in psychiatric disorders. Genetic mouse models have shown that 5-HT receptors and the 5-HT transporter acting during developmental stages modulate developmental processes. In addition, recent works demonstrated that appropriate 5-HT production and 5-HT degradation during develoment are needed for the development of 5-HT neurons and brain functions in the adult. In this review article, we focus on the importance of activities of tryptophan hydroxylase (TPH), the rate-limiting enzyme in 5-HT biosynthesis and monoamine oxidase A (MAOA), a catabolic enzyme responsible for deg- radation of 5-HT during development for the brain functions in the adult.","PeriodicalId":88753,"journal":{"name":"The open neuroscience journal","volume":"17 1","pages":"35-39"},"PeriodicalIF":0.0,"publicationDate":"2009-06-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"87451116","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":"Distal Tumors Elicit Distinctive Gene Expression Changes in Mouse Brain,Different from Those Induced by Arthritis","authors":"Mariano J. Alvarez, M. Salibe, G. Stolovitzky, M. Rubinstein, F. Pitossi, O. Podhajcer","doi":"10.2174/1874082000903010013","DOIUrl":"https://doi.org/10.2174/1874082000903010013","url":null,"abstract":"Background: Tumor progression is characterized by high mutation rates, each mutation potentially generating an \"alarm\" signal. The brain is the main integrator of signals arising in the periphery from changes in homeostasis. We hypothesized that tumors growing at a distant site might be a stimulus strong enough to be molecularly sensed and inte- grated by the brain. Results: Transcriptome analysis of the mouse hypothalamus, midbrain, and pre-fontal cortex at different time points fol- lowing administration at a distant site of mammary, lung and colon cancer cells evidenced cancer-type and brain-region specific changes in gene expression. On the contrary, no significant gene expression changes were detected in the liver. The hypothalamus was the region with the largest number of differentially expressed genes. On the array and off the array analysis of hypothalamic samples using real time PCR confirmed changes in genes associated with synaptic activity and sickness response, respectively. Gene clustering allowed the discrimination between each cancer model and between the cancer models and arthritis. Conclusions: The present data provides evidence of changes in gene expression in the brain during progression of distal tumors and arthritis highlighting a potential link between distal pathological processes and the brain.","PeriodicalId":88753,"journal":{"name":"The open neuroscience journal","volume":"19 1","pages":"13-25"},"PeriodicalIF":0.0,"publicationDate":"2009-06-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"73120792","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":"Activity-Dependent Axonal Plasticity: The Effects of Electrical Stimulation on Compound Action Potentials Recorded from the Mouse Nervous System In Vitro","authors":"Z. Ahmed, A. Wieraszko","doi":"10.2174/1874082000903010001","DOIUrl":"https://doi.org/10.2174/1874082000903010001","url":null,"abstract":"The influence of electrical stimulation on the amplitude of the action potentials recorded from the mouse nerv- ous system in vitro was investigated. Brief (1 s) high frequency (100 Hz) stimulation of the sciatic nerve induced a long- lasting increase in the amplitude of the compound action potential (CAP). Low frequency (1 Hz) stimulation delivered for 15 min attenuated the antidromically evoked potential recorded from hippocampal slices and CAP recorded from the sci- atic nerve. The stimulation-induced decrease in the amplitude of CAP occurred in two phases. While during the first phase the decrease was reversible and calcium-dependent, the second, later phase was irreversible. The experiments with two stimulating electrodes activated separately revealed that the changes in the CAP amplitude were not related to unspecific electrode-tissue interactions. The attenuation in the CAP amplitude was accompanied by an increase and decrease of minimal and maximal thresholds, respectively. The stimulation of the sciatic nerve segments with twin pulses revealed that the velocity of CAP propagation and refractoriness were significantly diminished after LFS application. The stimula- tion-induced changes in CAP were correlated with decreased sodium channels antibody signal, indicating fall in the num- ber of sodium channels. According to postulated hypothesis, the stimulation-induced influx of Na + during the first phase intensifies internalization of sodium channels. This amplified endocytosis is accompanied by activation of lysosomal pathways and subsequent hydrolysis of sodium channels leading to irreversible decline in the CAP amplitude. Described results indicate, that axons can contribute to neuronal plasticity.","PeriodicalId":88753,"journal":{"name":"The open neuroscience journal","volume":"11 1","pages":"1-12"},"PeriodicalIF":0.0,"publicationDate":"2009-04-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"74812510","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":"Ischemia Increases TREK-2 Channel Expression in Astrocytes: Relevance to Glutamate Clearance.","authors":"Lilia Y Kucheryavykh,&nbsp;Yuriy V Kucheryavykh,&nbsp;Mikhail Inyushin,&nbsp;Yaroslav M Shuba,&nbsp;Priscila Sanabria,&nbsp;Luis A Cubano,&nbsp;Serguei N Skatchkov,&nbsp;Misty J Eaton","doi":"10.2174/1874082000903010040","DOIUrl":"https://doi.org/10.2174/1874082000903010040","url":null,"abstract":"<p><p>The extent of an ischemic insult is less in brain regions enriched in astrocytes suggesting that astrocytes maintain function and buffer glutamate during ischemia. Astrocytes express a wide variety of potassium channels to support their functions including TREK-2 channels which are regulated by polyunsaturated fatty acids, intracellular acidosis and swelling; conditions that pertain to ischemia. The present study investigated the possible involvement of TREK-2 channels in cultured cortical astrocytes during experimental ischemia (anoxia/hypoglycemia) by examining TREK-2 protein levels, channel activity and ability to clear glutamate. We found that TREK-2 protein levels were increased rapidly within 2 hrs of the onset of simulated ischemia. This increase corresponded to an increase in temperature-sensitive TREK-2-like channel conductance and the ability of astrocytes to buffer extracellular glutamate even during ischemia. Together, these data suggest that up-regulation of TREK-2 channels may help rescue astrocyte function and lower extracellular glutamate during ischemia.</p>","PeriodicalId":88753,"journal":{"name":"The open neuroscience journal","volume":"3 ","pages":"40-47"},"PeriodicalIF":0.0,"publicationDate":"2009-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2771865/pdf/nihms139092.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"28489920","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Differential Expression of Redox Factor-1 Associated with Beta-Amyloid-Mediated Neurotoxicity.","authors":"Zhiqun Tan,&nbsp;Lei Shi,&nbsp;Steven S Schreiber","doi":"10.2174/1874082000903010026","DOIUrl":"https://doi.org/10.2174/1874082000903010026","url":null,"abstract":"<p><p>Redox factor-1 (Ref-1), also known as HAP1, APE or APEX, is a multifunctional protein that regulates gene transcription as well as the response to oxidative stress. By interacting with transcription factors such as AP-1, NF-kappaB and p53, and directly participating in the cleavage of apurininic/apyrimidinic DNA lesions, Ref-1 plays crucial roles in both cell death signaling pathways and DNA repair, respectively. Oxidative stress induced by aggregated beta-amyloid (Abeta) peptide, altered DNA repair and transcriptional activation of cell death pathways have been implicated in the pathophysiology of Alzheimer's disease (AD). Here we show that varying concentrations of Abeta(1-42) differentially regulate Ref-1 expression, Ref-1 function and neuronal survival in vitro. Abeta (5.0 muM) caused a relatively rapid decrease in Ref-1 expression and activity associated with extensive DNA damage and neuronal degeneration. In contrast, Ref-1 induction occurred in cells exposed to Abeta (1.0 muM) without significant neuronal cell death. Abeta-induced attenuation of Ref-1 expression and endonuclease activity, and neuronal cell death were prevented by the anti-oxidant, catalase. Similar differential effects on Ref-1 expression and cell viability were observed in N2A neuroblastoma cells treated with either high or low dose hydrogen peroxide. These findings demonstrate the differential regulation of Ref-1 expression by varying degrees of oxidative stress. Parallels between the Ref-1 response to Abeta and H(2)O(2) suggest similarities between DNA repair pathways activated by different inducers of oxidative stress. In AD brain, colocalization of Ref-1 and Abeta the absence of significant DNA damage are consistent with the cell culture results and suggests that Ref-1 may play a more neuroprotective role under these conditions. Modulation of Ref-1 expression and activity by local variations in Abeta concentration may be an important determinant of neuronal vulnerability to oxidative stress in AD.</p>","PeriodicalId":88753,"journal":{"name":"The open neuroscience journal","volume":"3 ","pages":"26-34"},"PeriodicalIF":0.0,"publicationDate":"2009-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2773510/pdf/nihms114639.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"28495825","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Actin and Actin-Binding Proteins: Masters of Dendritic Spine Formation, Morphology, and Function.","authors":"Wan-Hsin Lin, Donna J Webb","doi":"10.2174/1874082000903020054","DOIUrl":"10.2174/1874082000903020054","url":null,"abstract":"<p><p>Dendritic spines are actin-rich protrusions that comprise the postsynaptic sites of synapses and receive the majority of excitatory synaptic inputs in the central nervous system. These structures are central to cognitive processes, and alterations in their number, size, and morphology are associated with many neurological disorders. Although the actin cytoskeleton is thought to govern spine formation, morphology, and synaptic functions, we are only beginning to understand how modulation of actin reorganization by actin-binding proteins (ABPs) contributes to the function of dendritic spines and synapses. In this review, we discuss what is currently known about the role of ABPs in regulating the formation, morphology, motility, and plasticity of dendritic spines and synapses.</p>","PeriodicalId":88753,"journal":{"name":"The open neuroscience journal","volume":"3 ","pages":"54-66"},"PeriodicalIF":0.0,"publicationDate":"2009-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2921857/pdf/nihms224633.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"29194003","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Accelerators, Brakes, and Gears of Actin Dynamics in Dendritic Spines.","authors":"Crystal G Pontrello,&nbsp;Iryna M Ethell","doi":"10.2174/1874082000903020067","DOIUrl":"https://doi.org/10.2174/1874082000903020067","url":null,"abstract":"<p><p>Dendritic spines are actin-rich structures that accommodate the postsynaptic sites of most excitatory synapses in the brain. Although dendritic spines form and mature as synaptic connections develop, they remain plastic even in the adult brain, where they can rapidly grow, change, or collapse in response to normal physiological changes in synaptic activity that underlie learning and memory. Pathological stimuli can adversely affect dendritic spine shape and number, and this is seen in neurodegenerative disorders and some forms of mental retardation and autism as well. Many of the molecular signals that control these changes in dendritic spines act through the regulation of filamentous actin (F-actin), some through direct interaction with actin, and others via downstream effectors. For example, cortactin, cofilin, and gelsolin are actin-binding proteins that directly regulate actin dynamics in dendritic spines. Activities of these proteins are precisely regulated by intracellular signaling events that control their phosphorylation state and localization. In this review, we discuss how actin-regulating proteins maintain the balance between F-actin assembly and disassembly that is needed to stabilize mature dendritic spines, and how changes in their activities may lead to rapid remodeling of dendritic spines.</p>","PeriodicalId":88753,"journal":{"name":"The open neuroscience journal","volume":"3 ","pages":"67-86"},"PeriodicalIF":0.0,"publicationDate":"2009-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.2174/1874082000903020067","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"28983591","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Dendritic Spines: Similarities with Protrusions and Adhesions in Migrating Cells.","authors":"Miguel Vicente-Manzanares,&nbsp;Jennifer Hodges,&nbsp;Alan Rick Horwitz","doi":"10.2174/1874082000903020087","DOIUrl":"https://doi.org/10.2174/1874082000903020087","url":null,"abstract":"<p><p>Dendritic spines are specialized, micron-sized post-synaptic compartments that support synaptic function. These actin-based protrusions push the post-synaptic membrane, establish contact with the presynaptic membrane and undergo dynamic changes in morphology during development, as well as in response to synaptic neurotransmission. These processes are propelled by active remodeling of the actin cytoskeleton, which includes polymerization, filament disassembly, and organization of the actin in supramolecular arrays, such as branched networks or bundles. Dendritic spines contain a plethora of adhesion and synaptic receptors, signaling, and cytoskeletal proteins that regulate their formation, maturation and removal. Whereas many of the molecules involved in dendritic spine formation have been identified, their actual roles in spine formation, removal and maturation are not well understood. Using parallels between migrating fibroblasts and dendritic spines, we point to potential mechanisms and approaches for understanding spine development and dynamics.</p>","PeriodicalId":88753,"journal":{"name":"The open neuroscience journal","volume":"3 ","pages":"87-96"},"PeriodicalIF":0.0,"publicationDate":"2009-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2886280/pdf/nihms178002.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"29062574","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Spatiotemporal Regulation of Signaling in and out of Dendritic Spines: CaMKII and Ras.","authors":"Seok-Jin R Lee, Ryohei Yasuda","doi":"10.2174/1874082000903020117","DOIUrl":"10.2174/1874082000903020117","url":null,"abstract":"<p><p>Recent advances in 2-photon fluorescence lifetime imaging microscopy (2pFLIM) in combination with 2-photon photochemistry have enabled the visualization of neuronal signaling during synaptic plasticity at the level of single dendritic spines in light scattering tissue. Using these techniques, the activity of Ca(2+)/Calmodulin-dependent kinase II (CaMKII) and Ras have been imaged in single spines during synaptic plasticity and associated spine enlargement. These provide two contrasting examples of spatiotemporal regulation of spine signaling: Ras signaling is diffusive and spread over ~10 μm along the dendrites, while CaMKII activation is restricted to the spine undergoing plasticity. In this review, we will discuss the mechanisms and roles of the different spatiotemporal regulation of signaling in neurons, and the impact of the spine structure upon these biochemical signaling processes.</p>","PeriodicalId":88753,"journal":{"name":"The open neuroscience journal","volume":"3 ","pages":"117-127"},"PeriodicalIF":0.0,"publicationDate":"2009-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2867484/pdf/nihms174508.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"28983587","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}