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Journal articles on the topic 'Axonal ER'

Author: Grafiati

Published: 4 June 2021

Last updated: 3 February 2022

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1

Lee, Soyeon, Wei Wang, Jinyeon Hwang, Uk Namgung, and Kyung-Tai Min. "Increased ER–mitochondria tethering promotes axon regeneration." Proceedings of the National Academy of Sciences 116, no. 32 (2019): 16074–79. http://dx.doi.org/10.1073/pnas.1818830116.

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Translocation of the endoplasmic reticulum (ER) and mitochondria to the site of axon injury has been shown to facilitate axonal regeneration; however, the existence and physiological importance of ER–mitochondria tethering in the injured axons are unknown. Here, we show that a protein linking ER to mitochondria, the glucose regulated protein 75 (Grp75), is locally translated at axon injury site following axotomy, and that overexpression of Grp75 in primary neurons increases ER–mitochondria tethering to promote regrowth of injured axons. We find that increased ER–mitochondria tethering elevates

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2

Sun, Jingbo, Raihanah Harion, Tomoki Naito, and Yasunori Saheki. "INPP5K and Atlastin-1 maintain the nonuniform distribution of ER–plasma membrane contacts in neurons." Life Science Alliance 4, no. 11 (2021): e202101092. http://dx.doi.org/10.26508/lsa.202101092.

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In neurons, the ER extends throughout all cellular processes, forming multiple contacts with the plasma membrane (PM) to fine-tune neuronal physiology. However, the mechanisms that regulate the distribution of neuronal ER-PM contacts are not known. Here, we used the Caenorhabditis elegans DA9 motor neuron as our model system and found that neuronal ER-PM contacts are enriched in soma and dendrite and mostly absent in axons. Using forward genetic screen, we identified that the inositol 5-phosphatase, CIL-1 (human INPP5K), and the dynamin-like GTPase, ATLN-1 (human Atlastin-1), help to maintain

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3

Robinson, Richard. "Axonal Signaling Proteins Take the ER Highway." PLoS Biology 8, no. 10 (2010): e1000504. http://dx.doi.org/10.1371/journal.pbio.1000504.

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4

Lu, Meng, Francesca W. van Tartwijk, Julie Qiaojin Lin, et al. "The structure and global distribution of the endoplasmic reticulum network are actively regulated by lysosomes." Science Advances 6, no. 51 (2020): eabc7209. http://dx.doi.org/10.1126/sciadv.abc7209.

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The endoplasmic reticulum (ER) comprises morphologically and functionally distinct domains: sheets and interconnected tubules. These domains undergo dynamic reshaping in response to changes in the cellular environment. However, the mechanisms behind this rapid remodeling are largely unknown. Here, we report that ER remodeling is actively driven by lysosomes, following lysosome repositioning in response to changes in nutritional status: The anchorage of lysosomes to ER growth tips is critical for ER tubule elongation and connection. We validate this causal link via the chemo- and optogeneticall

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5

Glynn, Paul. "Axonal Degeneration and Neuropathy Target Esterase." Archives of Industrial Hygiene and Toxicology 58, no. 3 (2007): 355–58. http://dx.doi.org/10.2478/v10004-007-0029-z.

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Axonal Degeneration and Neuropathy Target EsteraseThis brief review summarises recent observations which suggest a possible mechanism for organophosphate-induced delayed neuropathy (OPIDN). Neuropathy target esterase (NTE) has been shown to deacylate endoplasmic reticulum (ER) membrane phosphatidylcholine (PtdCho). Raised levels of PtdCho are present in the brains of swiss cheese/NTE mutant Drosophila together with abnormal membrane structures, axonal and dendritic degeneration and neural cell loss. Similar vacuolated pathology is found in the brains of mice with brain-specific deletion of the

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6

Fuentes, Federico, and Carlos O. Arregui. "Microtubule and Cell Contact Dependency of ER-bound PTP1B Localization in Growth Cones." Molecular Biology of the Cell 20, no. 6 (2009): 1878–89. http://dx.doi.org/10.1091/mbc.e08-07-0675.

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PTP1B is an ER-bound protein tyrosine phosphatase implied in the regulation of cell adhesion. Here we investigated mechanisms involved in the positioning and dynamics of PTP1B in axonal growth cones and evaluated the role of this enzyme in axons. In growth cones, PTP1B consistently localizes in the central domain, and occasionally at the peripheral region and filopodia. Live imaging of GFP-PTP1B reveals dynamic excursions of fingerlike processes within the peripheral region and filopodia. PTP1B and GFP-PTP1B colocalize with ER markers and coalign with microtubules at the peripheral region and

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7

Gan, Kathlyn J., та Michael A. Silverman. "Dendritic and axonal mechanisms of Ca2+ elevation impair BDNF transport in Aβ oligomer–treated hippocampal neurons". Molecular Biology of the Cell 26, № 6 (2015): 1058–71. http://dx.doi.org/10.1091/mbc.e14-12-1612.

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Disruption of fast axonal transport (FAT) and intracellular Ca2+ dysregulation are early pathological events in Alzheimer's disease (AD). Amyloid-β oligomers (AβOs), a causative agent of AD, impair transport of BDNF independent of tau by nonexcitotoxic activation of calcineurin (CaN). Ca2+-dependent mechanisms that regulate the onset, severity, and spatiotemporal progression of BDNF transport defects from dendritic and axonal AβO binding sites are unknown. Here we show that BDNF transport defects in dendrites and axons are induced simultaneously but exhibit different rates of decline. The spat

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8

Allison, Rachel, James R. Edgar, Guy Pearson, et al. "Defects in ER–endosome contacts impact lysosome function in hereditary spastic paraplegia." Journal of Cell Biology 216, no. 5 (2017): 1337–55. http://dx.doi.org/10.1083/jcb.201609033.

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Contacts between endosomes and the endoplasmic reticulum (ER) promote endosomal tubule fission, but the mechanisms involved and consequences of tubule fission failure are incompletely understood. We found that interaction between the microtubule-severing enzyme spastin and the ESCRT protein IST1 at ER–endosome contacts drives endosomal tubule fission. Failure of fission caused defective sorting of mannose 6-phosphate receptor, with consequently disrupted lysosomal enzyme trafficking and abnormal lysosomal morphology, including in mouse primary neurons and human stem cell–derived neurons. Consi

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9

Tabb, J. S., B. J. Molyneaux, D. L. Cohen, S. A. Kuznetsov, and G. M. Langford. "Transport of ER vesicles on actin filaments in neurons by myosin V." Journal of Cell Science 111, no. 21 (1998): 3221–34. http://dx.doi.org/10.1242/jcs.111.21.3221.

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Axoplasmic organelles in the giant axon of the squid have been shown to move on both actin filaments and microtubules and to switch between actin filaments and microtubules during fast axonal transport. The objectives of this investigation were to identify the specific classes of axoplasmic organelles that move on actin filaments and the myosin motors involved. We developed a procedure to isolate endoplasmic reticulum (ER) from extruded axoplasm and to reconstitute its movement in vitro. The isolated ER vesicles moved on exogenous actin filaments adsorbed to coverslips in an ATP-dependent mann

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10

Wang, Bingjie, You Yu, Lai Wei, and Yan Zhang. "Inhibition of ER stress improves progressive motor deficits in a REEP1-null mouse model of hereditary spastic paraplegia." Biology Open 9, no. 9 (2020): bio054296. http://dx.doi.org/10.1242/bio.054296.

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ABSTRACTHereditary spastic paraplegias (HSPs) are genetic neurodegenerative diseases. HSPs are characterized by lower-extremity weakness and spasticity. However, there is no specific clinical treatment strategy to prevent or reverse nerve degeneration in HSPs. Mutations in receptor expression-enhancing protein 1 (REEP1) are well-recognized and relatively common causes of autosomal dominant HSPs. REEP1 modifies the endoplasmic reticulum (ER) shape, and is implicated in the ER stress response. Defects in the ER stress response seem to be crucial mechanisms underlying HSP neurodegeneration. Here,

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11

Ying, Zhengxin, Vikram Misra, and Valerie M. K. Verge. "Sensing nerve injury at the axonal ER: Activated Luman/CREB3 serves as a novel axonally synthesized retrograde regeneration signal." Proceedings of the National Academy of Sciences 111, no. 45 (2014): 16142–47. http://dx.doi.org/10.1073/pnas.1407462111.

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12

Hetzer, Shelby M., Fernanda Guilhaume-Correa, Dylan Day, Alicia Bedolla, and Nathan K. Evanson. "Traumatic Optic Neuropathy Is Associated with Visual Impairment, Neurodegeneration, and Endoplasmic Reticulum Stress in Adolescent Mice." Cells 10, no. 5 (2021): 996. http://dx.doi.org/10.3390/cells10050996.

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Traumatic brain injury (TBI) results in a number of impairments, often including visual symptoms. In some cases, visual impairments after head trauma are mediated by traumatic injury to the optic nerve, termed traumatic optic neuropathy (TON), which has few effective options for treatment. Using a murine closed-head weight-drop model of head trauma, we previously reported in adult mice that there is relatively selective injury to the optic tract and thalamic/brainstem projections of the visual system. In the current study, we performed blunt head trauma on adolescent C57BL/6 mice and investiga

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13

Gallo, Alessandra, Lydia Danglot, Francesca Giordano, et al. "Role of the Sec22b–E-Syt complex in neurite growth and ramification." Journal of Cell Science 133, no. 18 (2020): jcs247148. http://dx.doi.org/10.1242/jcs.247148.

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ABSTRACTAxons and dendrites are long and often ramified neurites that need particularly intense plasma membrane (PM) expansion during the development of the nervous system. Neurite growth depends on non-fusogenic Sec22b–Stx1 SNARE complexes at endoplasmic reticulum (ER)–PM contacts. Here, we show that Sec22b interacts with members of the extended synaptotagmin (E-Syt) family of ER lipid transfer proteins (LTPs), and this interaction depends on the longin domain of Sec22b. Overexpression of E-Syts stabilizes Sec22b–Stx1 association, whereas silencing of E-Syts has the opposite effect. Overexpre

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14

Krols, Michiel, Bob Asselbergh, Riet De Rycke, et al. "Sensory neuropathy-causing mutations in ATL3 affect ER–mitochondria contact sites and impair axonal mitochondrial distribution." Human Molecular Genetics 28, no. 4 (2018): 615–27. http://dx.doi.org/10.1093/hmg/ddy352.

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15

Parakh, Sonam, Damian M. Spencer, Mark A. Halloran, Kai Y. Soo, and Julie D. Atkin. "Redox Regulation in Amyotrophic Lateral Sclerosis." Oxidative Medicine and Cellular Longevity 2013 (2013): 1–12. http://dx.doi.org/10.1155/2013/408681.

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Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease that results from the death of upper and lower motor neurons. Due to a lack of effective treatment, it is imperative to understand the underlying mechanisms and processes involved in disease progression. Regulations in cellular reduction/oxidation (redox) processes are being increasingly implicated in disease. Here we discuss the possible involvement of redox dysregulation in the pathophysiology of ALS, either as a cause of cellular abnormalities or a consequence. We focus on its possible role in oxidative stress, protein misfo

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16

Greaves, Erin, Frances Collins, Arantza Esnal-Zufiaurre, Sevasti Giakoumelou, Andrew W. Horne, and Philippa T. K. Saunders. "Estrogen Receptor (ER) Agonists Differentially Regulate Neuroangiogenesis in Peritoneal Endometriosis via the Repellent Factor SLIT3." Endocrinology 155, no. 10 (2014): 4015–26. http://dx.doi.org/10.1210/en.2014-1086.

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Abstract Endometriosis is an estrogen-dependent neurovascular disorder characterized by growth of endometrial tissue (lesions) outside the uterine cavity. Patients suffer chronic pelvic pain, and it has been proposed that co-recruitment of nerves/blood vessels (neuroangiogenesis) into the lesions is fundamental to the development of painful symptoms. We hypothesized that estrogen-dependent regulation of axonal guidance molecules of the SLIT/ROBO (Roundabout) family could play a role in neuroangiogenesis occurring in endometriosis lesions found on the peritoneal wall. In tissue samples from hum

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17

Connell, James W., Rachel J. Allison, Catherine E. Rodger, Guy Pearson, Eliska Zlamalova, and Evan Reid. "ESCRT-III-associated proteins and spastin inhibit protrudin-dependent polarised membrane traffic." Cellular and Molecular Life Sciences 77, no. 13 (2019): 2641–58. http://dx.doi.org/10.1007/s00018-019-03313-z.

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Abstract Mutations in the gene encoding the microtubule severing ATPase spastin are the most frequent cause of hereditary spastic paraplegia, a genetic condition characterised by length-dependent axonal degeneration. Here, we show that HeLa cells lacking spastin and embryonic fibroblasts from a spastin knock-in mouse model become highly polarised and develop cellular protrusions. In HeLa cells, this phenotype was rescued by wild-type spastin, but not by forms unable to sever microtubules or interact with endosomal ESCRT-III proteins. Cells lacking the spastin-interacting ESCRT-III-associated p

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18

Tang, Leo T. H., Meera Trivedi, Jenna Freund, et al. "The CATP-8/P5A-type ATPase functions in multiple pathways during neuronal patterning." PLOS Genetics 17, no. 7 (2021): e1009475. http://dx.doi.org/10.1371/journal.pgen.1009475.

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The assembly of neuronal circuits involves the migrations of neurons from their place of birth to their final location in the nervous system, as well as the coordinated growth and patterning of axons and dendrites. In screens for genes required for patterning of the nervous system, we identified the catp-8/P5A-ATPase as an important regulator of neural patterning. P5A-ATPases are part of the P-type ATPases, a family of proteins known to serve a conserved function as transporters of ions, lipids and polyamines in unicellular eukaryotes, plants, and humans. While the function of many P-type ATPa

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19

Argueti-Ostrovsky, Shirel, Leenor Alfahel, Joy Kahn, and Adrian Israelson. "All Roads Lead to Rome: Different Molecular Players Converge to Common Toxic Pathways in Neurodegeneration." Cells 10, no. 9 (2021): 2438. http://dx.doi.org/10.3390/cells10092438.

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Multiple neurodegenerative diseases (NDDs) such as Alzheimer’s disease (AD), Parkinson’s disease (PD), amyotrophic lateral sclerosis (ALS) and Huntington’s disease (HD) are being suggested to have common cellular and molecular pathological mechanisms, characterized mainly by protein misfolding and aggregation. These large inclusions, most likely, represent an end stage of a molecular cascade; however, the soluble misfolded proteins, which take part in earlier steps of this cascade, are the more toxic players. These pathological proteins, which characterize each specific disease, lead to the se

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20

Bedry, Tuji, and Henok Tadele. "Pattern and Outcome of Pediatric Traumatic Brain Injury at Hawassa University Comprehensive Specialized Hospital, Southern Ethiopia: Observational Cross-Sectional Study." Emergency Medicine International 2020 (January 29, 2020): 1–9. http://dx.doi.org/10.1155/2020/1965231.

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Background. Traumatic brain injury (TBI) is the most common cause of death/disability in children. The Glasgow coma scale and other parameters are used for treatment/follow-up of TBI. Childhood TBI data are scarce from sub-Saharan Africa. The study aimed to determine the pattern and predictors of the TBI outcome in Southern Ethiopia. Methods. An observational cross-sectional study was conducted from September 2017 to September 2018 at Hawassa University Hospital. Structured questionnaires were used for data collection. Significant associations were declared at a P value of <0.05. Results. T

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21

Liu, Xiaomei, Qing Zhang, Weixiao Wang, et al. "Analysis of Long Noncoding RNA and mRNA Expression Profiles in IL-9-Activated Astrocytes and EAE Mice." Cellular Physiology and Biochemistry 45, no. 5 (2018): 1986–98. http://dx.doi.org/10.1159/000487975.

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Background/Aims: Multiple sclerosis (MS) is an autoimmune disease in the central nervous system associated with demyelination and axonal injury. Astrocyte activation is involved in the pathogenesis of MS and experimental autoimmune encephalomyelitis (EAE), an animal model of MS. This study was designed to find potential lncRNAs in EAE mice and activated astrocytes. Methods: we performed microarray analysis of lncRNAs from the brain tissues of EAE mice and primary mouse astrocytes treated with IL-9(50 ng/ml). 12 lncRNAs were validated through real-time PCR. Gene ontology and KEGG pathway analys

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Walton, P. D., J. A. Airey, J. L. Sutko, et al. "Ryanodine and inositol trisphosphate receptors coexist in avian cerebellar Purkinje neurons." Journal of Cell Biology 113, no. 5 (1991): 1145–57. http://dx.doi.org/10.1083/jcb.113.5.1145.

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Two intracellular calcium-release channel proteins, the inositol trisphosphate (InsP3), and ryanodine receptors, have been identified in mammalian and avian cerebellar Purkinje neurons. In the present study, biochemical and immunological techniques were used to demonstrate that these proteins coexist in the same avian Purkinje neurons, where they have different intracellular distributions. Western analyses demonstrate that antibodies produced against the InsP3 and the ryanodine receptors do not cross-react. Based on their relative rates of sedimentation in continuous sucrose gradients and SDS-

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23

Sharma, Govinda, Rasha Sabouny, Matthew Joel, et al. "Characterization of a novel variant in the HR1 domain of MFN2 in a patient with ataxia, optic atrophy and sensorineural hearing loss." F1000Research 10 (July 19, 2021): 606. http://dx.doi.org/10.12688/f1000research.53230.1.

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Background: Pathogenic variants in MFN2 cause Charcot-Marie-Tooth disease (CMT) type 2A (CMT2A) and are the leading cause of the axonal subtypes of CMT. CMT2A is characterized by predominantly distal motor weakness and muscle atrophy, with highly variable severity and onset age. Notably, some MFN2 variants can also lead to other phenotypes such as optic atrophy, hearing loss and lipodystrophy. Despite the clear link between MFN2 and CMT2A, our mechanistic understanding of how dysfunction of the MFN2 protein causes human disease pathologies remains incomplete. This lack of understanding is due

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24

Wu, Yumei, Christina Whiteus, C. Shan Xu, et al. "Contacts between the endoplasmic reticulum and other membranes in neurons." Proceedings of the National Academy of Sciences 114, no. 24 (2017): E4859—E4867. http://dx.doi.org/10.1073/pnas.1701078114.

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Close appositions between the membrane of the endoplasmic reticulum (ER) and other intracellular membranes have important functions in cell physiology. These include lipid homeostasis, regulation of Ca2+ dynamics, and control of organelle biogenesis and dynamics. Although these membrane contacts have previously been observed in neurons, their distribution and abundance have not been systematically analyzed. Here, we have used focused ion beam-scanning electron microscopy to generate 3D reconstructions of intracellular organelles and their membrane appositions involving the ER (distance ≤30 nm)

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25

Eward, William C., Carter Lipton, Jonathan Barnwell, Thomas L. Smith, Matthew Crowe, and L. Andrew Koman. "Nerve Conduit Enhancement with Vomeronasal Organ Improves Rat Sciatic Functional Index in a Segmental Nerve Defect Model." Duke Orthopaedic Journal 1, no. 1 (2011): 9–15. http://dx.doi.org/10.5005/jp-journals-10017-1002.

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ABSTRACT Background Segmental nerve loss presents a challenge to the reconstructive surgeon. The best regenerative results are obtained by using autologous interpositional nerve grafts. While this method can be successful, it necessitates a second surgical step, sacrifices donor nerve function and depends upon a finite supply of potential donor nerves. Collagen nerve conduits are commercially available for reconstruction of segmental nerve defects. However, no conduit-based reconstructive strategy has been as successful as autograft reconstruction. We hypothesized that collagen nerve conduits

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Rao, Kavitha, Michelle C. Stone, Alexis T. Weiner, et al. "Spastin, atlastin, and ER relocalization are involved in axon but not dendrite regeneration." Molecular Biology of the Cell 27, no. 21 (2016): 3245–56. http://dx.doi.org/10.1091/mbc.e16-05-0287.

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Mutations in >50 genes, including spastin and atlastin, lead to hereditary spastic paraplegia (HSP). We previously demonstrated that reduction of spastin leads to a deficit in axon regeneration in a Drosophila model. Axon regeneration was similarly impaired in neurons when HSP proteins atlastin, seipin, and spichthyin were reduced. Impaired regeneration was dependent on genetic background and was observed when partial reduction of HSP proteins was combined with expression of dominant-negative microtubule regulators, suggesting that HSP proteins work with microtubules to promote regeneration

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Lee, Soyeon, Wei Wang, Jinyeon Hwang, U. K. Namgung, and Kyung-Tai Min. "Increased ER–mitochondria tethering promotes axon regeneration." IBRO Reports 6 (September 2019): S213. http://dx.doi.org/10.1016/j.ibror.2019.07.664.

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28

Verkhratsky, Alexei. "Physiology and Pathophysiology of the Calcium Store in the Endoplasmic Reticulum of Neurons." Physiological Reviews 85, no. 1 (2005): 201–79. http://dx.doi.org/10.1152/physrev.00004.2004.

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The endoplasmic reticulum (ER) is the largest single intracellular organelle, which is present in all types of nerve cells. The ER is an interconnected, internally continuous system of tubules and cisterns, which extends from the nuclear envelope to axons and presynaptic terminals, as well as to dendrites and dendritic spines. Ca2+release channels and Ca2+pumps residing in the ER membrane provide for its excitability. Regulated ER Ca2+release controls many neuronal functions, from plasmalemmal excitability to synaptic plasticity. Enzymatic cascades dependent on the Ca2+concentration in the ER

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29

Almey, Anne, Edward J. Filardo, Teresa A. Milner, and Wayne G. Brake. "Estrogen Receptors Are Found in Glia and at Extranuclear Neuronal Sites in the Dorsal Striatum of Female Rats: Evidence for Cholinergic But Not Dopaminergic Colocalization." Endocrinology 153, no. 11 (2012): 5373–83. http://dx.doi.org/10.1210/en.2012-1458.

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Abstract Estrogens rapidly affect dopamine (DA) neurotransmission in the dorsal striatum (dSTR) and DA-related diseases, such as Parkinson's disease and schizophrenia. How estrogens influence DA function remains unclear, in part, because the ultrastructural localization of estrogen receptors (ER) in the dSTR is not known. Light microscopic studies of the dSTR have suggested the presence of ER. This experiment used electron microscopy to determine whether these ER are at extranuclear sites in the dSTR, providing evidence for a mechanism through which estrogen could rapidly affect DA transmissio

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Aridor, Meir, and Kenneth N. Fish. "Selective Targeting of ER Exit Sites Supports Axon Development." Traffic 10, no. 11 (2009): 1669–84. http://dx.doi.org/10.1111/j.1600-0854.2009.00974.x.

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Krijnse-Locker, J., R. G. Parton, S. D. Fuller, G. Griffiths, and C. G. Dotti. "The organization of the endoplasmic reticulum and the intermediate compartment in cultured rat hippocampal neurons." Molecular Biology of the Cell 6, no. 10 (1995): 1315–32. http://dx.doi.org/10.1091/mbc.6.10.1315.

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The boundaries of the organelles of the biosynthetic endomembrane system are still controversial. In this paper we take advantage of the unique architectural organization of neurons to investigate the localization of a spectrum of compartment-specific markers with the goal of defining the location of the rough endoplasmic reticulum (ER), smooth ER, intermediate compartment, and the Golgi complex. Markers of the rough ER (signal sequence receptor), Golgi complex (mannosidase II), and the trans Golgi network (TGN38) were essentially restricted to the cell body and the initial segment of one of t

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Pacheco, Almudena, and Jeffery L. Twiss. "Localized IRES-Dependent Translation of ER Chaperone Protein mRNA in Sensory Axons." PLoS ONE 7, no. 7 (2012): e40788. http://dx.doi.org/10.1371/journal.pone.0040788.

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Renvoisé, Benoît, and Craig Blackstone. "Emerging themes of ER organization in the development and maintenance of axons." Current Opinion in Neurobiology 20, no. 5 (2010): 531–37. http://dx.doi.org/10.1016/j.conb.2010.07.001.

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Fowler, Philippa C., Dwayne J. Byrne, Craig Blackstone, and Niamh C. O'Sullivan. "Loss of the Mitochondrial Fission GTPase Drp1 Contributes to Neurodegeneration in a Drosophila Model of Hereditary Spastic Paraplegia." Brain Sciences 10, no. 9 (2020): 646. http://dx.doi.org/10.3390/brainsci10090646.

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Mitochondrial morphology, distribution and function are maintained by the opposing forces of mitochondrial fission and fusion, the perturbation of which gives rise to several neurodegenerative disorders. The large guanosine triphosphate (GTP)ase dynamin-related protein 1 (Drp1) is a critical regulator of mitochondrial fission by mediating membrane scission, often at points of mitochondrial constriction at endoplasmic reticulum (ER)-mitochondrial contacts. Hereditary spastic paraplegia (HSP) subtype SPG61 is a rare neurodegenerative disorder caused by mutations in the ER-shaping protein Arl6IP1

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Page, Stephen J., Scott E. Kasner, Marcia Bockbrader, et al. "A double-blind, randomized, controlled study of two dose strengths of dalfampridine extended release on walking deficits in ischemic stroke." Restorative Neurology and Neuroscience 38, no. 4 (2020): 301–9. http://dx.doi.org/10.3233/rnn-201009.

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Background: Stroke-induced ischemia affects both cortex and underlying white matter. Dalfampridine extended release tablets (D-ER) enhance action potential conduction in demyelinated axons, which may positively affect post-stroke recovery. Objective: Based on promising preliminary data, we compared efficacy of D-ER administered at 7.5 mg or 10 mg with placebo on post-stroke ambulation. Primary study outcome (response) was a ≥20% increase on the 2-minute walk test (2 MinWT) at 12 weeks after first drug administration. Methods: This was a multicenter, randomized, placebo-controlled, 3-arm, paral

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Neufeld, Janina, Gertraud Teuchert-Noodt, Keren Grafen, York Winter, and A. Veronica Witte. "Synapse Plasticity in Motor, Sensory, and Limbo-Prefrontal Cortex Areas as Measured by Degrading Axon Terminals in an Environment Model of Gerbils (Meriones unguiculatus)." Neural Plasticity 2009 (2009): 1–14. http://dx.doi.org/10.1155/2009/281561.

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Still little is known about naturally occurring synaptogenesis in the adult neocortex and related impacts of epigenetic influences. We therefore investigated (pre)synaptic plasticity in various cortices of adult rodents, visualized by secondary lysosome accumulations (LA) in remodeling axon terminals. Twenty-two male gerbils from either enriched (ER) or impoverished rearing (IR) were used for quantification of silver-stained LA. ER-animals showed rather low LA densities in most primary fields, whereas barrel and secondary/associative cortices exhibited higher densities and layer-specific diffe

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Lee, Jee Y., Soo Y. Choi, Tae H. Oh та Tae Y. Yune. "17β-Estradiol Inhibits Apoptotic Cell Death of Oligodendrocytes by Inhibiting RhoA-JNK3 Activation after Spinal Cord Injury". Endocrinology 153, № 8 (2012): 3815–27. http://dx.doi.org/10.1210/en.2012-1068.

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A delayed oligodendrocyte cell death after spinal cord injury (SCI) contributes to chronic demyelination of spared axons, leading to a permanent neurological deficit. Therefore, therapeutic approaches to prevent oligodendrocyte cell death after SCI should be considered. Estrogens are well known to have a broad neuroprotective effect, but the protective effect of estrogens on oligodendrocytes after injury is largely unknown. Here, we demonstrated that 17β-estradiol attenuates apoptosis of oligodendrocytes by inhibiting RhoA and c-Jun-N-terminal kinase activation after SCI. Estrogen receptor (ER

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Wei, Ran, Arika Sugiyama, Yuta Sato, et al. "Isoform-dependent subcellular localization of LMTK1A and LMTK1B and their roles in axon outgrowth and spine formation." Journal of Biochemistry 168, no. 1 (2020): 23–32. http://dx.doi.org/10.1093/jb/mvaa019.

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Abstract Lemur kinase 1 (LMTK1) is a membrane-bound Ser/Thr kinase that is expressed in neurons. There are two splicing variants of LMTK1 with different membrane binding modes, viz., cytosolic LMTK1A that binds to membranes through palmitoylation at the N-terminal cysteines and LMTK1B, an integral membrane protein with transmembrane sequences. We recently reported that LMTK1A regulates axon outgrowth and spine formation in neurons. However, data about LMTK1B are scarce. We analysed the expression and cellular localization of LMTK1B along with its role in axon and spine formation. We found that

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Bonnon, Carine, Christophe Bel, Laurence Goutebroze, Bernard Maigret, Jean-Antoine Girault, and Catherine Faivre-Sarrailh. "PGY Repeats and N-Glycans Govern the Trafficking of Paranodin and Its Selective Association with Contactin and Neurofascin-155." Molecular Biology of the Cell 18, no. 1 (2007): 229–41. http://dx.doi.org/10.1091/mbc.e06-06-0570.

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Formation of nodes of Ranvier requires contact of axons with myelinating glial cells, generating specialized axo-glial subdomains. Caspr/paranodin is required for the formation of septate-like junctions at paranodes, whereas the related caspr2 is essential for the organization of juxtaparanodes. The molecular mechanisms underlying the segregation of these related glycoproteins within distinct complexes are poorly understood. Exit of paranodin from the endoplasmic reticulum (ER) is mediated by its interaction with F3/contactin. Using domain swapping with caspr2, we mapped a motif with Pro-Gly-T

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Villa, A., P. Podini, D. O. Clegg, T. Pozzan, and J. Meldolesi. "Intracellular Ca2+ stores in chicken Purkinje neurons: differential distribution of the low affinity-high capacity Ca2+ binding protein, calsequestrin, of Ca2+ ATPase and of the ER lumenal protein, Bip." Journal of Cell Biology 113, no. 4 (1991): 779–91. http://dx.doi.org/10.1083/jcb.113.4.779.

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To identify intracellular Ca2+ stores, we have mapped (by cryosection immunofluorescence and immunogold labeling) the distribution in the chicken cerebellar cortex of an essential component, the main low affinity-high capacity Ca2+ binding protein which in this tissue has been recently shown undistinguishable from muscle calsequestrin (Volpe, P., B. H. Alderson-Lang, L. Madeddu, E. Damiani, J. H. Collins, and A. Margreth. 1990. Neuron. 5:713-721). Appreciable levels of the protein were found exclusively within Purkinje neurons, distributed to the cell body, the axon, and the elaborate dendriti

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Pare, D., R. C. Dossi, and M. Steriade. "Three types of inhibitory postsynaptic potentials generated by interneurons in the anterior thalamic complex of cat." Journal of Neurophysiology 66, no. 4 (1991): 1190–204. http://dx.doi.org/10.1152/jn.1991.66.4.1190.

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1. These experiments were carried out to study how thalamic interneurons generate inhibitory postsynaptic potentials (IPSPs) in relay cells. Intracellular recordings were performed in the anterior thalamic (AT) nuclei, a nuclear group in which interneurons constitute the only intrathalamic source of gamma-aminobutyric acid (GABA). 2. In the AT complex, as in most dorsal thalamic nuclei, interneurons can influence relay cells through their presynaptic dendrites (PSDs) and their axons. This dual mode of action is paralleled by a different termination pattern of prethalamic fibers and cortical ax

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Zhang, Xiao-Feng, and Paul Forscher. "Rac1 Modulates Stimulus-evoked Ca2+ Release in Neuronal Growth Cones via Parallel Effects on Microtubule/Endoplasmic Reticulum Dynamics and Reactive Oxygen Species Production." Molecular Biology of the Cell 20, no. 16 (2009): 3700–3712. http://dx.doi.org/10.1091/mbc.e08-07-0730.

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The small G protein Rac regulates cytoskeletal protein dynamics in neuronal growth cones and has been implicated in axon growth, guidance, and branching. Intracellular Ca2+ is another well known regulator of growth cone function; however, effects of Rac activity on intracellular Ca2+ metabolism have not been well characterized. Here, we investigate how Rac1 activity affects release of Ca2+ from intracellular endoplasmic reticulum (ER) stores stimulated by application of serotonin (5-hydroxytriptamine). We also address how Rac1 effects on microtubule assembly dynamics affect distribution of Ca2

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Chang, Hui-Yi, Chen-Li Cheng, Jia-Jin J. Chen, and William C. de Groat. "Roles of glutamatergic and serotonergic mechanisms in reflex control of the external urethral sphincter in urethane-anesthetized female rats." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 291, no. 1 (2006): R224—R234. http://dx.doi.org/10.1152/ajpregu.00780.2005.

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This study was conducted to examine reflex mechanisms that mediate urinary bladder and external urethral sphincter (EUS) coordination in urethane-anesthetized female Sprague-Dawley rats. We investigated the properties of EUS reflexes elicited by electrical stimulation of pelvic nerve afferent axons (pelvic-EUS reflex). The changes in the reflexes induced by bladder distension and administration of agonists or antagonists for glutamatergic or serotonergic receptors were examined. The reflexes consisted of an early response (ER, 18- to 22-ms latency) and a late, long-duration (>100-ms latency

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Paul, Mandy H., Myoung Choi, Jessica Schlaudraff, Thomas Deller, and Domenico Del Turco. "Granule Cell Ensembles in Mouse Dentate Gyrus Rapidly Upregulate the Plasticity-Related Protein Synaptopodin after Exploration Behavior." Cerebral Cortex 30, no. 4 (2019): 2185–98. http://dx.doi.org/10.1093/cercor/bhz231.

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Abstract The plasticity-related protein Synaptopodin (SP) has been implicated in neuronal plasticity. SP is targeted to dendritic spines and the axon initial segment, where it organizes the endoplasmic reticulum (ER) into the spine apparatus and the cisternal organelle, respectively. Here, we report an inducible third localization of SP in the somata of activated granule cell ensembles in mouse dentate gyrus. Using immunofluorescence and fluorescence in situ hybridization, we observed a subpopulation of mature granule cells (~1–2%) exhibiting perinuclear SP protein and a strong somatic SP mRNA

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Ogino, Kazutoyo, Sean E. Low, Kenta Yamada, et al. "RING finger protein 121 facilitates the degradation and membrane localization of voltage-gated sodium channels." Proceedings of the National Academy of Sciences 112, no. 9 (2015): 2859–64. http://dx.doi.org/10.1073/pnas.1414002112.

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Following their synthesis in the endoplasmic reticulum (ER), voltage-gated sodium channels (NaV) are transported to the membranes of excitable cells, where they often cluster, such as at the axon initial segment of neurons. Although the mechanisms by which NaV channels form and maintain clusters have been extensively examined, the processes that govern their transport and degradation have received less attention. Our entry into the study of these processes began with the isolation of a new allele of the zebrafish mutant alligator, which we found to be caused by mutations in the gene encoding r

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Almey, Anne, Elizabeth Cannell, Kyla Bertram, Edward Filardo, Teresa A. Milner, and Wayne G. Brake. "Medial Prefrontal Cortical Estradiol Rapidly Alters Memory System Bias in Female Rats: Ultrastructural Analysis Reveals Membrane-Associated Estrogen Receptors as Potential Mediators." Endocrinology 155, no. 11 (2014): 4422–32. http://dx.doi.org/10.1210/en.2014-1463.

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Abstract High plasma levels of estradiol (E2) are associated with use of a place memory system over a response memory system. We examined whether infusing estradiol into the medial prefrontal cortex (mPFC) or anterior cingulate cortex (AC) could affect memory system bias in female rats. We also examined the ultrastructural distribution of estrogen receptor (ER)-α, ERβ, and G protein-coupled estrogen receptor 1 (GPER1) in the mPFC of female rats as a mechanism for the behavioral effects of E2 in the mPFC. Each rat was infused bilaterally with either E2 (0.13 μg) or vehicle into the mPFC or AC.

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Montenegro, Gladys, Adriana P. Rebelo, James Connell, et al. "Mutations in the ER-shaping protein reticulon 2 cause the axon-degenerative disorder hereditary spastic paraplegia type 12." Journal of Clinical Investigation 122, no. 2 (2012): 538–44. http://dx.doi.org/10.1172/jci60560.

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Rao, Mala V., Panaiyur S. Mohan, Asok Kumar, et al. "The Myosin Va Head Domain Binds to the Neurofilament-L Rod and Modulates Endoplasmic Reticulum (ER) Content and Distribution within Axons." PLoS ONE 6, no. 2 (2011): e17087. http://dx.doi.org/10.1371/journal.pone.0017087.

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Tsukahara, Shinji, and Korehito Yamanouchi. "Sex Difference in Septal Neurons Projecting Axons to Midbrain Central Gray in Rats: A Combined Double Retrograde Tracing and ER-Immunohistochemical Study." Endocrinology 143, no. 1 (2002): 285–94. http://dx.doi.org/10.1210/endo.143.1.8588.

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Chang, Hui-Yi, Chen-Li Cheng, Jia-Jin J. Chen, and William C. de Groat. "Serotonergic drugs and spinal cord transections indicate that different spinal circuits are involved in external urethral sphincter activity in rats." American Journal of Physiology-Renal Physiology 292, no. 3 (2007): F1044—F1053. http://dx.doi.org/10.1152/ajprenal.00175.2006.

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Lower urinary tract function is regulated by spinal and supraspinal reflexes that coordinate the activity of the urinary bladder and external urethral sphincter (EUS). Two types of EUS activity (tonic and bursting) have been identified in rats. This study in urethane-anesthetized female rats used cystometry, EUS electromyography, spinal cord transection (SCT) at different segmental levels, and analysis of the effects of 5-HT1A receptor agonist (8-OH-DPAT) and antagonist (WAY100635) drugs to examine the origin of tonic and bursting EUS activity. EUS activity was elicited by bladder distension o

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