Journal articles: 'Dendrite degeneration'

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Lin, Chin-Hsien, Hsun Li, Yi-Nan Lee, Ying-Ju Cheng, Ruey-Meei Wu, and Cheng-Ting Chien. "Lrrk regulates the dynamic profile of dendritic Golgi outposts through the golgin Lava lamp." Journal of Cell Biology 210, no. 3 (July 27, 2015): 471–83. http://dx.doi.org/10.1083/jcb.201411033.

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Constructing the dendritic arbor of neurons requires dynamic movements of Golgi outposts (GOPs), the prominent component in the dendritic secretory pathway. GOPs move toward dendritic ends (anterograde) or cell bodies (retrograde), whereas most of them remain stationary. Here, we show that Leucine-rich repeat kinase (Lrrk), the Drosophila melanogaster homologue of Parkinson’s disease–associated Lrrk2, regulates GOP dynamics in dendrites. Lrrk localized at stationary GOPs in dendrites and suppressed GOP movement. In Lrrk loss-of-function mutants, anterograde movement of GOPs was enhanced, whereas Lrrk overexpression increased the pool size of stationary GOPs. Lrrk interacted with the golgin Lava lamp and inhibited the interaction between Lva and dynein heavy chain, thus disrupting the recruitment of dynein to Golgi membranes. Whereas overexpression of kinase-dead Lrrk caused dominant-negative effects on GOP dynamics, overexpression of the human LRRK2 mutant G2019S with augmented kinase activity promoted retrograde movement. Our study reveals a pathogenic pathway for LRRK2 mutations causing dendrite degeneration.

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Yang, Wei-Kang, and Cheng-Ting Chien. "Beyond being innervated: the epidermis actively shapes sensory dendritic patterning." Open Biology 9, no. 3 (March 2019): 180257. http://dx.doi.org/10.1098/rsob.180257.

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Sensing environmental cues requires well-built neuronal circuits linked to the body surface. Sensory neurons generate dendrites to innervate surface epithelium, thereby making it the largest sensory organ in the body. Previous studies have illustrated that neuronal type, physiological function and branching patterns are determined by intrinsic factors. Perhaps for effective sensation or protection, sensory dendrites bind to or are surrounded by the substrate epidermis. Recent studies have shed light on the mechanisms by which dendrites interact with their substrates. These interactions suggest that substrates can regulate dendrite guidance, arborization and degeneration. In this review, we focus on recent studies of Drosophila and Caenorhabditis elegans that demonstrate how epidermal cells can regulate dendrites in several aspects.

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Bauer, Carol A., Thomas J. Brozoski, and Kristin Myers. "Primary afferent dendrite degeneration as a cause of tinnitus." Journal of Neuroscience Research 85, no. 7 (2007): 1489–98. http://dx.doi.org/10.1002/jnr.21259.

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TRIBBLE, JAMES R., STEPHEN D. CROSS, PAULINA A. SAMSEL, FRANK SENGPIEL, and JAMES E. MORGAN. "A novel system for the classification of diseased retinal ganglion cells." Visual Neuroscience 31, no. 6 (November 2014): 373–80. http://dx.doi.org/10.1017/s0952523814000248.

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AbstractRetinal ganglion cell (RGC) dendritic atrophy is an early feature of many forms of retinal degeneration, providing a challenge to RGC classification. The characterization of these changes is complicated by the possibility that selective labeling of any particular class can confound the estimation of dendritic remodeling. To address this issue we have developed a novel, robust, and quantitative RGC classification based on proximal dendritic features which are resistant to early degeneration. RGCs were labeled through the ballistic delivery of DiO and DiI coated tungsten particles to whole retinal explants of 20 adult Brown Norway rats. RGCs were grouped according to the Sun classification system. A comprehensive set of primary and secondary dendrite features were quantified and a new classification model derived using principal component (PCA) and discriminant analyses, to estimate the likelihood that a cell belonged to any given class. One-hundred and thirty one imaged RGCs were analyzed; according to the Sun classification, 24% (n = 31) were RGCA, 29% (n = 38) RGCB, 32% (n = 42) RGCC, and 15% (n = 20) RGCD. PCA gave a 3 component solution, separating RGCs based on descriptors of soma size and primary dendrite thickness, proximal dendritic field size and dendritic tree asymmetry. The new variables correctly classified 73.3% (n = 74) of RGCs from a training sample and 63.3% (n = 19) from a hold out sample indicating an effective model. Soma and proximal dendritic tree morphological features provide a useful surrogate measurement for the classification of RGCs in disease. While a definitive classification is not possible in every case, the technique provides a useful safeguard against sample bias where the normal criteria for cell classification may not be reliable.

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Chopra, Ravi, David D. Bushart, and Vikram G. Shakkottai. "Dendritic potassium channel dysfunction may contribute to dendrite degeneration in spinocerebellar ataxia type 1." PLOS ONE 13, no. 5 (May 30, 2018): e0198040. http://dx.doi.org/10.1371/journal.pone.0198040.

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Koike, Tatsuro, Yi Yang, Kazuhiko Suzuki, and Xiaoxiang Zheng. "Axon & dendrite degeneration: Its mechanisms and protective experimental paradigms." Neurochemistry International 52, no. 4-5 (March 2008): 751–60. http://dx.doi.org/10.1016/j.neuint.2007.09.007.

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Azizah, Nurul, Sisca Sisca, and Rasiha Rasiha. "REGENERASI DENDRIT SEL GANGLION RETINA: PERAN INSULIN UNTUK MENGEMBALIKAN PENGLIHATAN PADA GLAUKOMA." Al-Iqra Medical Journal : Jurnal Berkala Ilmiah Kedokteran 1, no. 2 (November 12, 2019): 74–83. http://dx.doi.org/10.26618/aimj.v1i2.2758.

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Glaukoma is a leading cause of irreversible blindness worldwide. This disease is associated with characteristic damage to the optic nerve and permanent retinal ganglion cell (RGC) degeneration. A crucial step towards circuit repair in glaucoma is to promote damaged RGCs to regenerate not only axons, but also dendrites to successfully reconnect with their synaptic partners. The latest research showed that insulin signalling has the capacity to regenerate dendrites dan injured synapses, therefore the use of insulin raises a new paradigm as a new pro-regenerative therapeutic target for the disease of glaucoma. This literature review is made using literature searching of valid journals with inclusion and exclusion criteria. On the experiment of insulin’s effectivity, it is valued using 4 indicators; promote dendrite regeneration, restore synaptic density, rescue retinal function, robust neuronal survival. Based on in vivo experiment, insulin endowed with the ability to effectively restore dendritic morphology thus enhancing the function and survival of RGC through mTORC1 (mammalian target of rapamycin complex 1) and mTORC2 (mammalian target of rapamycin complex 2) signalling, this supports that that it can be promising therapeutic targets to counter progressive RGC neurodegeneration and vision loss in glaucoma.

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Satoh, Daisuke, Ritsuko Suyama, Ken‐ichi Kimura, and Tadashi Uemura. "High‐resolution in vivo imaging of regenerating dendrites of D rosophila sensory neurons during metamorphosis: local filopodial degeneration and heterotypic dendrite–dendrite contacts." Genes to Cells 17, no. 12 (November 15, 2012): 939–51. http://dx.doi.org/10.1111/gtc.12008.

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Plowey, Edward D., Jon W. Johnson, Erin Steer, Wan Zhu, David A. Eisenberg, Natalie M. Valentino, Yong-Jian Liu, and Charleen T. Chu. "Mutant LRRK2 enhances glutamatergic synapse activity and evokes excitotoxic dendrite degeneration." Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease 1842, no. 9 (September 2014): 1596–603. http://dx.doi.org/10.1016/j.bbadis.2014.05.016.

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Kolotov, K. A., and P. G. Rasputin. "MONOCYTIC CHEMOTACTIC PROTEIN-1 IN PHYSIOLOGY AND MEDICINE (REVIEW OF LITERATURE)." Perm Medical Journal 35, no. 3 (December 15, 2018): 99–105. http://dx.doi.org/10.17816/pmj35399-105.

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Monocytic chemotactic protein-1-cytokin, attributed to the group of chemokins, is the most powerful factor of monocyte chemotaxis in the body of mammalians as well as memory T-cells and dendrite cells to inflammatory foci and is produced upon tissue damages or infection introduced. MCP-1 is mainly secreted by monocytes, macrophages and dendrite cells. Clinical significance of MCP-1 consists in participation of some diseases in pathogenesis: psoriasis, rheumatoid arthritis, atherosclerosis. MCP-1 is involved into the processes of developing central nervous system diseases, which are characterized by neuronal degeneration. Besides, this cytokine plays a significant role in vascular complications of type 2 diabetes mellitus and formation of obesity insulin resistance.

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Rosidi, Nathanael L., Joan Zhou, Sanket Pattanaik, Peng Wang, Weiyang Jin, Morgan Brophy, William L. Olbricht, Nozomi Nishimura, and Chris B. Schaffer. "Cortical Microhemorrhages Cause Local Inflammation but Do Not Trigger Widespread Dendrite Degeneration." PLoS ONE 6, no. 10 (October 19, 2011): e26612. http://dx.doi.org/10.1371/journal.pone.0026612.

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Li, Xi, Yves Fautrelle, Rene Moreau, and Zhongming Ren. "EBSD study of the morphology and orientation of the primary and eutectic phases in Al–Cu alloys during solidification under a strong magnetic field." Journal of Applied Crystallography 49, no. 1 (February 1, 2016): 139–48. http://dx.doi.org/10.1107/s1600576715021731.

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The effect of a strong magnetic field on the morphology and orientation of the Al2Cu dendrite and Al–Al2Cu eutectic in Al–Cu alloys was studied using electron backscatter diffraction (EBSD) technology. The experimental results revealed that the applied magnetic field modified the morphology and orientation of both the Al2Cu dendrite and the Al–Al2Cu eutectic significantly. The magnetic field caused a break in the Al2Cu dendrite and the degeneration of Al–Al2Cu eutectic lamellae during directional solidification. It was also found that the magnetic field caused the formation of dislocations in the α-Al and Al2Cu phases during directional solidification. In addition, the primary and eutectic Al2Cu phases were oriented with the 〈001〉 crystal direction along the magnetic field during volume solidification. Both α-Al and Al2Cu phases were oriented with the 〈001〉 crystal direction along the solidification direction during directional solidification under an axial magnetic field. The above phenomena were enhanced as the magnetic field increased; this could be attributed to magnetic crystalline anisotropy of the material and thermoelectric magnetic effects. This study may offer experimental evidence that shows that thermoelectric magnetic effects significantly influence dendrite arrays during directional solidification in a magnetic field.

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Wen, Yuhui, R. Grace Zhai, and Michael D. Kim. "The role of autophagy in Nmnat-mediated protection against hypoxia-induced dendrite degeneration." Molecular and Cellular Neuroscience 52 (January 2013): 140–51. http://dx.doi.org/10.1016/j.mcn.2012.11.008.

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Tao, Juan, Chengye Feng, and Melissa M. Rolls. "The microtubule-severing protein fidgetin acts after dendrite injury to promote their degeneration." Journal of Cell Science 129, no. 17 (July 13, 2016): 3274–81. http://dx.doi.org/10.1242/jcs.188540.

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Fukui, Koji, Keisuke Ushiki, Hirokatsu Takatsu, Tatsuro Koike, and Shiro Urano. "Tocotrienols prevent hydrogen peroxide-induced axon and dendrite degeneration in cerebellar granule cells." Free Radical Research 46, no. 2 (January 23, 2012): 184–93. http://dx.doi.org/10.3109/10715762.2011.647689.

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Greenough, William T., John W. McDonald, Robert M. Parnisari, and James E. Camel. "Environmental conditions modulate degeneration and new dendrite growth in cerebellum of senescent rats." Brain Research 380, no. 1 (August 1986): 136–43. http://dx.doi.org/10.1016/0006-8993(86)91437-x.

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Serdar, Mordelt, Müser, Kempe, Felderhoff-Müser, Herz, and Bendix. "Detrimental Impact of Energy Drink Compounds on Developing Oligodendrocytes and Neurons." Cells 8, no. 11 (November 3, 2019): 1381. http://dx.doi.org/10.3390/cells8111381.

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The consumption of energy drinks is continuously rising, particularly in children and adolescents. While risks for adverse health effects, like arrhythmia, have been described, effects on neural cells remain elusive. Considering that neurodevelopmental processes like myelination and neuronal network formation peak in childhood and adolescence we hypothesized that developing oligodendrocytes and neurons are particularly vulnerable to main energy drink components. Immature oligodendrocytes and hippocampal neurons were isolated from P0-P1 Wistar rats and were incubated with 0.3 mg/mL caffeine and 4 mg/mL taurine alone or in combination for 24 h. Analysis was performed immediately after treatment or after additional three days under differentiating conditions for oligodendrocytes and standard culture for neurons. Oligodendrocyte degeneration, proliferation, and differentiation were assessed via immunocytochemistry and immunoblotting. Neuronal integrity was investigated following immunocytochemistry by analysis of dendrite outgrowth and axonal morphology. Caffeine and taurine induced an increased degeneration and inhibited proliferation of immature oligodendrocytes accompanied by a decreased differentiation capacity. Moreover, dendritic branching and axonal integrity of hippocampal neurons were negatively affected by caffeine and taurine treatment. The negative impact of caffeine and taurine on developing oligodendrocytes and disturbed neuronal morphology indicates a high risk for disturbed neurodevelopment in children and adolescents by excessive energy drink consumption.

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E, Lezi, Ting Zhou, Sehwon Koh, Marian Chuang, Ruchira Sharma, Nathalie Pujol, Andrew D. Chisholm, Cagla Eroglu, Hiroaki Matsunami, and Dong Yan. "An Antimicrobial Peptide and Its Neuronal Receptor Regulate Dendrite Degeneration in Aging and Infection." Neuron 97, no. 1 (January 2018): 125–38. http://dx.doi.org/10.1016/j.neuron.2017.12.001.

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Verma, Manish, Jason Callio, P. Anthony Otero, Israel Sekler, Zachary P. Wills, and Charleen T. Chu. "Mitochondrial Calcium Dysregulation Contributes to Dendrite Degeneration Mediated by PD/LBD-Associated LRRK2 Mutants." Journal of Neuroscience 37, no. 46 (October 16, 2017): 11151–65. http://dx.doi.org/10.1523/jneurosci.3791-16.2017.

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Kaur, Supender, and Alejandro Aballay. "G-Protein-Coupled Receptor SRBC-48 Protects against Dendrite Degeneration and Reduced Longevity Due to Infection." Cell Reports 31, no. 7 (May 2020): 107662. http://dx.doi.org/10.1016/j.celrep.2020.107662.

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Zhao, Shu, Xiang Gao, Weiren Dong, and Jinhui Chen. "The Role of 7,8-Dihydroxyflavone in Preventing Dendrite Degeneration in Cortex After Moderate Traumatic Brain Injury." Molecular Neurobiology 53, no. 3 (March 24, 2015): 1884–95. http://dx.doi.org/10.1007/s12035-015-9128-z.

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Lin, C. H., P. I. Tsai, R. M. Wu, and C. T. Chien. "LRRK2 G2019S Mutation Induces Dendrite Degeneration through Mislocalization and Phosphorylation of Tau by Recruiting Autoactivated GSK3." Journal of Neuroscience 30, no. 39 (September 29, 2010): 13138–49. http://dx.doi.org/10.1523/jneurosci.1737-10.2010.

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Jara, Javier H., Stephanie R. Villa, Nabil A. Khan, Martha C. Bohn, and P. Hande Özdinler. "AAV2 mediated retrograde transduction of corticospinal motor neurons reveals initial and selective apical dendrite degeneration in ALS." Neurobiology of Disease 47, no. 2 (August 2012): 174–83. http://dx.doi.org/10.1016/j.nbd.2012.03.036.

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Knoll, Renata M., Reuven Ishai, Danielle R. Trakimas, Jenny X. Chen, Joseph B. Nadol, Steven D. Rauch, Aaron K. Remenschneider, David H. Jung, and Elliott D. Kozin. "Peripheral Vestibular System Histopathologic Changes following Head Injury without Temporal Bone Fracture." Otolaryngology–Head and Neck Surgery 160, no. 1 (October 2, 2018): 122–30. http://dx.doi.org/10.1177/0194599818795695.

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Objective Vestibular symptoms such as dizziness and vertigo are common after head injury and may be due to trauma to the peripheral vestibular system. The pathophysiology of peripheral vestibular symptoms following head injury without temporal bone (TB) fracture, however, is not well understood. Herein, we investigate the histopathology of the peripheral vestibular system of patients who sustained head injury without a TB fracture. Study Design Otopathology study. Setting Otopathology laboratory. Subjects and Methods TB of subjects with a history of head injury without TB fractures were included and evaluated by light microscopy. Specimens were assessed for qualitative and quantitative characteristics, such as number of Scarpa’s ganglion cells in the superior and inferior vestibular nerves, vestibular hair cell and/or dendrite degeneration in vestibular end organs, presence of vestibular hydrops, and obstruction of the endolymphatic duct. Results Five cases (n = 5 TBs) had evidence of vestibular pathology. There was a decrease of 48.6% (range, 40%-59%) in the mean count of Scarpa’s ganglion cells as compared with that of normative historical age-matched controls. Moderate to severe degeneration of the vestibular membranous labyrinth was identified in the posterior, superior, and lateral canals in several cases (50%, n = 4 TBs). The maculae utriculi and sacculi showed mild to severe degeneration in 2 cases. Additional findings include vestibular hydrops (25%, n = 2 TBs) and blockage of the endolymphatic duct (n = 1 TB). Conclusions Otopathologic analysis of patients with a history of head injury without TB fracture demonstrated peripheral vestibular otopathology. Future studies are necessary to determine if otopathology findings are directly attributable to head injury.

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de Pádua Lima Filho, Antonio, and Rafael Shoiti Ikeda. "Continuous Production of Metal Matrix Composites from the Semisolid State." Solid State Phenomena 192-193 (October 2012): 83–88. http://dx.doi.org/10.4028/www.scientific.net/ssp.192-193.83.

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Continuous strip metal matrix composite (MMC) casting of 0.3 mm diameter hard-drawn stainless steel (316L) wire in a quasi-eutectic SnPb (64Sn36Pb) matrix was performed by a two-roll melt drag processing (TRMDping) method, with the wire being dragged through a semisolid puddle with a fibre contact time of approximately 0.2 s. A slag weir placed at the nozzle contained two wire guide holes: one located near the upper roll, and the other located between the rolls. A successful continuous composite strip casting with good fibre alignment was achieved by inserting and embedding the wire into the matrix using the guide hole between the rolls. Degeneration of eutectic/dendrite structures led to the formation of globular structures. The occurrence and formation mechanisms of cracks, de-lamination and voids in the matrix were discussed. TRMDping is economically viable and has significant benefits over other MMC fabrication methods.

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Friedman, L. G., M. L. Lachenmayer, J. Wang, L. He, S. M. Poulose, M. Komatsu, G. R. Holstein, and Z. Yue. "Disrupted Autophagy Leads to Dopaminergic Axon and Dendrite Degeneration and Promotes Presynaptic Accumulation of -Synuclein and LRRK2 in the Brain." Journal of Neuroscience 32, no. 22 (May 30, 2012): 7585–93. http://dx.doi.org/10.1523/jneurosci.5809-11.2012.

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Malacrida, Alessio, Cristina Meregalli, Virginia Rodriguez-Menendez, and Gabriella Nicolini. "Chemotherapy-Induced Peripheral Neuropathy and Changes in Cytoskeleton." International Journal of Molecular Sciences 20, no. 9 (May 9, 2019): 2287. http://dx.doi.org/10.3390/ijms20092287.

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Despite the different antineoplastic mechanisms of action, peripheral neurotoxicity induced by all chemotherapy drugs (anti-tubulin agents, platinum compounds, proteasome inhibitors, thalidomide) is associated with neuron morphological changes ascribable to cytoskeleton modifications. The “dying back” degeneration of distal terminals (sensory nerves) of dorsal root ganglia sensory neurons, observed in animal models, in in vitro cultures and biopsies of patients is the most evident hallmark of the perturbation of the cytoskeleton. On the other hand, in highly polarized cells like neurons, the cytoskeleton carries out its role not only in axons but also has a fundamental role in dendrite plasticity and in the organization of soma. In the literature, there are many studies focused on the antineoplastic-induced alteration of microtubule organization (and consequently, fast axonal transport defects) while very few studies have investigated the effect of the different classes of drugs on microfilaments, intermediate filaments and associated proteins. Therefore, in this review, we will focus on: (1) Highlighting the fundamental role of the crosstalk among the three filamentous subsystems and (2) investigating pivotal cytoskeleton-associated proteins.

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Blagburn, J. M., D. J. Beadle, and D. B. Sattelle. "Development of synapses between identified sensory neurones and giant interneurones in the cockroach Periplaneta americana." Development 86, no. 1 (April 1, 1985): 227–46. http://dx.doi.org/10.1242/dev.86.1.227.

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The cereal afferent, giant interneurone pathway in Periplaneta americana was used as a model for synapse formation. The morphology of the two identified filiform hair sensory neurones (FHSNs) and of two giant interneurones (GI2 and GI3) was followed throughout embryogenesis by cobalt injection. The FHSN axons enter the CNS at the 45 % stage of embryogenesis, branch at 50 % and form complete arborizations by 70 %. The giant interneurones send out a primary dendrite at 45 %. Secondary branches form between 50 % and 60 % and elaboration of the branching pattern takes place until 80 % embryogenesis. At early stages the FHSN axons are within filopodial range of GI dendrites which may use these sensory processes as guidance cues. Synapse formation between the main FHSN axon shafts and GI dendrites was investigated by injection of the latter with HRP. From 55 % to 65 % the process is initiated by desmosome—like filopodial contacts, with subsequent vesicle clustering and formation of a small synaptic density. Numbers of contacts did not significantly increase after about 70 %, but the number of synapses doubled between 65 % and 75 %, with each GI process becoming postsynaptic to two FHSN synapses and the presynaptic densities lengthening to become bars. From 75 % embryogenesis to hatching there is a further small increase in synaptic bar length. In the first instar GI3 is postsynaptic to both FHSN axons, whereas GI2 forms very few synapses with the axon of the lateral FHSN (LFHSN). This imbalance of contacts is present throughout synaptogenesis, apart from some early filopodial contacts. GI3 forms synapses with the lateral side of the LFHSN axon from 60 % embryogenesis but these are totally absent at hatching. The growth of glia along this side of the axon during the last 30 % of development appears to be associated with degeneration of synapses in this region. Thus, as the dendrites of the GIs grow to form a miniature version of the adult without loss of branches, there is little evidence of an initial overproduction of FHSN—GI synapses. Similarly there is no evidence that GI2 forms ‘incorrect’ synapses with the axon of LFHSN. However, GI3 contacts are removed from an inappropriate region of a correct synaptic partner, LFHSN.

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Arsović, Aleksandar, Melanie Vanessa Halbach, Júlia Canet-Pons, Dilhan Esen-Sehir, Claudia Döring, Florian Freudenberg, Nicoletta Czechowska, et al. "Mouse Ataxin-2 Expansion Downregulates CamKII and Other Calcium Signaling Factors, Impairing Granule—Purkinje Neuron Synaptic Strength." International Journal of Molecular Sciences 21, no. 18 (September 12, 2020): 6673. http://dx.doi.org/10.3390/ijms21186673.

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Spinocerebellar ataxia type 2 (SCA2) is caused by polyglutamine expansion in Ataxin-2 (ATXN2). This factor binds RNA/proteins to modify metabolism after stress, and to control calcium (Ca2+) homeostasis after stimuli. Cerebellar ataxias and corticospinal motor neuron degeneration are determined by gain/loss in ATXN2 function, so we aimed to identify key molecules in this atrophic process, as potential disease progression markers. Our Atxn2-CAG100-Knock-In mouse faithfully models features observed in patients at pre-onset, early and terminal stages. Here, its cerebellar global RNA profiling revealed downregulation of signaling cascades to precede motor deficits. Validation work at mRNA/protein level defined alterations that were independent of constant physiological ATXN2 functions, but specific for RNA/aggregation toxicity, and progressive across the short lifespan. The earliest changes were detected at three months among Ca2+ channels/transporters (Itpr1, Ryr3, Atp2a2, Atp2a3, Trpc3), IP3 metabolism (Plcg1, Inpp5a, Itpka), and Ca2+-Calmodulin dependent kinases (Camk2a, Camk4). CaMKIV–Sam68 control over alternative splicing of Nrxn1, an adhesion component of glutamatergic synapses between granule and Purkinje neurons, was found to be affected. Systematic screening of pre/post-synapse components, with dendrite morphology assessment, suggested early impairment of CamKIIα abundance together with the weakening of parallel fiber connectivity. These data reveal molecular changes due to ATXN2 pathology, primarily impacting excitability and communication.

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Lee, Sangmook, WonHee Kim, Zhihan Li, and Garth F. Hall. "Accumulation of Vesicle-Associated Human Tau in Distal Dendrites Drives Degeneration and Tau Secretion in anIn SituCellular Tauopathy Model." International Journal of Alzheimer's Disease 2012 (2012): 1–16. http://dx.doi.org/10.1155/2012/172837.

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We used a nontransgenic cellular tauopathy model in which individual giant neurons in the lamprey CNS (ABCs) overexpress human tau isoforms cell autonomously to characterize the still poorly understood consequences of disease-associated tau processingin situ. In this model, tau colocalizes with endogenous microtubules and is nontoxic when expressed at low levels, but is misprocessed by a toxicity-associated alternative pathway when expressed above levels that saturate dendritic microtubules, causing abnormally phosphorylated, vesicle-associated tau to accumulate in ABC distal dendrites. This causes localized microtubule loss and eventually dendritic degeneration, which is preceded by tau secretion to the extracellular space. This sequence is reiterated at successively more proximal dendritic locations over time, suggesting that tau-induced dendritic degeneration is driven by distal dendritic accumulation of hyperphosphorylated, vesicle-associated tau perpetuated by localized microtubule loss. The implications for the diagnosis and treatment of human disease are discussed.

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Hall, G. F., B. Chu, G. Lee, and J. Yao. "Human tau filaments induce microtubule and synapse loss in an in vivo model of neurofibrillary degenerative disease." Journal of Cell Science 113, no. 8 (April 15, 2000): 1373–87. http://dx.doi.org/10.1242/jcs.113.8.1373.

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The intracellular accumulation of tau protein and its aggregation into filamentous deposits is the intracellular hallmark of neurofibrillary degenerative diseases such as Alzheimer's Disease and familial tauopathies in which tau is now thought to play a critical pathogenic role. Until very recently, the lack of a cellular model in which human tau filaments can be experimentally generated has prevented direct investigation of the causes and consequences of tau filament formation in vivo. In this study, we show that human tau filaments formed in lamprey central neurons (ABCs) that chronically overexpress human tau resemble the ‘straight filaments’ seen in Alzheimer's Disease and other neurofibrillary conditions, and are distinguishable from neurofilaments by their ultrastructure, distribution and intracellular behavior. We also show that tau filament formation in ABCs is associated with a distinctive pattern of dendritic degeneration that closely resembles the cytopathology of human neurofibrillary degenerative disease. This pattern includes localized cytoskeletal disruption and aggregation of membranous organelles, distal dendritic beading, and the progressive loss of dendritic microtubules and synapses. These results suggest that tau filament formation may be responsible for many key cytopathological features of neurofibrillary degeneration, possibly via the loss of microtubule based intracellular transport.

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Imbriani, Paola, Annalisa Tassone, Maria Meringolo, Giulia Ponterio, Graziella Madeo, Antonio Pisani, Paola Bonsi, and Giuseppina Martella. "Loss of Non-Apoptotic Role of Caspase-3 in the PINK1 Mouse Model of Parkinson’s Disease." International Journal of Molecular Sciences 20, no. 14 (July 11, 2019): 3407. http://dx.doi.org/10.3390/ijms20143407.

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Caspases are a family of conserved cysteine proteases that play key roles in multiple cellular processes, including programmed cell death and inflammation. Recent evidence shows that caspases are also involved in crucial non-apoptotic functions, such as dendrite development, axon pruning, and synaptic plasticity mechanisms underlying learning and memory processes. The activated form of caspase-3, which is known to trigger widespread damage and degeneration, can also modulate synaptic function in the adult brain. Thus, in the present study, we tested the hypothesis that caspase-3 modulates synaptic plasticity at corticostriatal synapses in the phosphatase and tensin homolog (PTEN) induced kinase 1 (PINK1) mouse model of Parkinson’s disease (PD). Loss of PINK1 has been previously associated with an impairment of corticostriatal long-term depression (LTD), rescued by amphetamine-induced dopamine release. Here, we show that caspase-3 activity, measured after LTD induction, is significantly decreased in the PINK1 knockout model compared with wild-type mice. Accordingly, pretreatment of striatal slices with the caspase-3 activator α-(Trichloromethyl)-4-pyridineethanol (PETCM) rescues a physiological LTD in PINK1 knockout mice. Furthermore, the inhibition of caspase-3 prevents the amphetamine-induced rescue of LTD in the same model. Our data support a hormesis-based double role of caspase-3; when massively activated, it induces apoptosis, while at lower level of activation, it modulates physiological phenomena, like the expression of corticostriatal LTD. Exploring the non-apoptotic activation of caspase-3 may contribute to clarify the mechanisms involved in synaptic failure in PD, as well as in view of new potential pharmacological targets.

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Pereiro, Xandra, Noelia Ruzafa, J. Haritz Urcola, Sansar C. Sharma, and Elena Vecino. "Differential Distribution of RBPMS in Pig, Rat, and Human Retina after Damage." International Journal of Molecular Sciences 21, no. 23 (December 7, 2020): 9330. http://dx.doi.org/10.3390/ijms21239330.

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RNA binding protein with multiple splicing (RBPMS) is expressed exclusively in retinal ganglion cells (RGCs) in the retina and can label all RGCs in normal retinas of mice, rats, guinea pigs, rabbits, cats, and monkeys, but its function in these cells is not known. As a result of the limited knowledge regarding RBPMS, we analyzed the expression of RBPMS in the retina of different mammalian species (humans, pigs, and rats), in various stages of development (neonatal and adult) and with different levels of injury (control, hypoxia, and organotypic culture or explants). In control conditions, RBPMS was localized in the RGCs somas in the ganglion cell layer, whereas in hypoxic conditions, it was localized in the RGCs dendrites in the inner plexiform layer. Such differential distributions of RBPMS occurred in all analyzed species, and in adult and neonatal retinas. Furthermore, we demonstrate RBPMS localization in the degenerating RGCs axons in the nerve fiber layer of retinal explants. This is the first evidence regarding the possible transport of RBPMS in response to physiological damage in a mammalian retina. Therefore, RBPMS should be further investigated in relation to its role in axonal and dendritic degeneration.

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Risner, Michael L., Silvia Pasini, Melissa L. Cooper, Wendi S. Lambert, and David J. Calkins. "Axogenic mechanism enhances retinal ganglion cell excitability during early progression in glaucoma." Proceedings of the National Academy of Sciences 115, no. 10 (February 20, 2018): E2393—E2402. http://dx.doi.org/10.1073/pnas.1714888115.

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Diseases of the brain involve early axon dysfunction that often precedes outright degeneration. Pruning of dendrites and their synapses represents a potential driver of axonopathy by reducing activity. Optic nerve degeneration in glaucoma, the world’s leading cause of irreversible blindness, involves early stress to retinal ganglion cell (RGC) axons from sensitivity to intraocular pressure (IOP). This sensitivity also influences survival of RGC dendrites and excitatory synapses in the retina. Here we tested in individual RGCs identified by type the relationship between dendritic organization and axon signaling to light following modest, short-term elevations in pressure. We found dendritic pruning occurred early, by 2 wk of elevation, and independent of whether the RGC responded to light onset (ON cells) or offset (OFF cells). Pruning was similarly independent of ON and OFF in the DBA/2J mouse, a chronic glaucoma model. Paradoxically, all RGCs, even those with significant pruning, demonstrated a transient increase in axon firing in response to the preferred light stimulus that occurred on a backdrop of generally enhanced excitability. The increased response was not through conventional presynaptic signaling, but rather depended on voltage-sensitive sodium channels that increased transiently in the axon. Pruning, axon dysfunction, and deficits in visual acuity did not progress between 2 and 4 wk of elevation. These results suggest neurodegeneration in glaucoma involves an early axogenic response that counters IOP-related stress to excitatory dendritic architecture to slow progression and maintain signaling to the brain. Thus, short-term exposure to elevated IOP may precondition the neural system to further insult.

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Hámori, József, Robert L. Jakab, and József Takács. "Morphogenetic Plasticity of Neuronal Elements in Cerebellar Glomeruli during Deafferentation-Induced Synaptic Reorganization." Journal of Neural Transplantation and Plasticity 6, no. 1 (1997): 11–20. http://dx.doi.org/10.1155/np.1997.11.

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Reorganization of the cerebellar glomerulus, the main synaptic complex within the granule cell layer, was investigated using quantitative morphological techniques. All afferents to the cerebellar cortex, including mossy-fibers, were surgically destroyed by undercutting the cerebellar vermis. Fifteen days after the operation, which resulted in the removal of the main excitatory afferent to the glomerulus, a significant reorganization of the whole synaptic complex was observed, whereas the structural integrity of the glomerulus was remarkably well preserved. This was indicated by the observation that the number of granule cell dendrites (≈50 per glomerulus), as well as the number of dendritic digits (≈210 per glomerulus) bearing most of the ≈230 synaptic junctions per glomerulus, did not change significantly after mossy-fiber degeneration. The total number of synapses in the reorganized glomerulus did not change either, despite the disappearance of two-thirds of (excitatory) synaptic junctions caused by mossy-fiber degeneration. In the reorganized glomeruli, however, the inhibitory, GABA-containing Golgi axonal varicosities became the dominant synaptic type—about four-fifths (≈200) of all synapses within the glomerulus—whereas the dendritic synapses between the granule cells represented only one-fifth of all synaptic junctions. The quantitative data of the reorganized cerebellar glomerulus demonstrate both a remarkable constancy and a plasticity of he excitatory granule cells and inhibitory Golgi neurons building up this synaptic complex. constancy (the preservation of certain specific structural features) is represented by an eventually unchanged number of dendrites and synaptic junctions within the deafferented lomerulus. Such constancy was made possible, however, by the morphogenetic plasticity of both nerve-cell types to produce new, dendrodendritic and axo-dendritic synapses to compensate for the loss of mossy-fiber synapses.

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Zhuravleva, Z. N. "Ultrastructural Signs of Regenerative-Degenerative Processes in Long-Term Dentate Fascia Grafts." Journal of Neural Transplantation and Plasticity 5, no. 3 (1994): 183–97. http://dx.doi.org/10.1155/np.1994.183.

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An ultrastructural investigation of embryonic (E20) dentate fascia grafts transplanted into an acute cavity in the somatosensory neocortex of adult rats revealed a continuous dynamic state of the tissue nine months postgrafting. The grafts consisted mainly of typical granular cells with some admixture of hippocampal pyramidal neurons and polymorph hilar cells with a normal, mature ultrastructure. Many features of the transplanted tissue suggested continuing development and growth. Dendritic branches with growth tips, axonal growth cones, synaptic boutons with growth vesicles, immature myelin sheaths and myelin-producing cells were observed. In contrast, ultrastructural signs of degeneration were present in some axons, and, less often, in dendrites. These processes, as well as some of the terminal synapses, contained various amounts of lysosomes and lipofuscine granules. In many such terminals the signs of degenerative change were combined with the presence of multiple mitochondria, polymorph vesicles and tubular reticulum, indicating simultaneous reparative processes. It is suggested that continuous recycling of neuronal processes occurs in longterm dentate grafts. This morphological instability nay depend on the paucity of synaptic targets within the dentate tissue transplanted with a minimal quantity of hippocampal pyramidal cells and on the limitation of the afferent input. However, the observed features of the grafted dentate tissue are not qualitatively different from those observed in normal dentate with its protracted development and active compensatory reorganization.

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Yamada, Tatsuo, Haruhiko Akiyama, and Patrick L. McGeer. "Two Types of Spheroid Bodies in the Nigral Neurons in Parkinson's Disease." Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 18, no. 3 (August 1991): 287–94. http://dx.doi.org/10.1017/s0317167100031838.

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ABSTRACT:Dendritic spheroid bodies (SBs) and Lewy bodies (LBs) were identified in comparable numbers in the substantia nigra pars compacta (SBC) of nine parkinsonian cases and one case of striatonigral degeneration but were not found irt cases of Huntington's disease or neurologically normal controls. The immunohistochemical profile of the SBs in dystrophic dendrites of nigrostriatal dopaminergic neurons was remarkably similar to that of the LBs found within dendrites or free of the SNC neuropil. Both types of inclusions stained positively with antibodies to tyrosine hydroxylase, ubiquitin and microtubule-associated protein-2 (MAP2), and negatively for Tau-2, although they had different ultrastructural appearances. A few intracellular LBs were stained by antibodies to neurofilament proteins (NFs) 68, 160, and 200 kD, but dendritic SBs and extracellular LBs were not so stained. These data indicate that dendritic SBs and extracellular LBs may have a common molecular pathogenetic origin in Parkinson's disease. On the other hand, the SBs seen in the pars reticulata (SNR) and in the distal nigrostriatal axons even in control cases were generally stained by antibodies to NFs and ubiquitin but not to MAP2. This latter staining pattern in similar to that shown by SBs in the anterior horn in ALS and in the cerebellum of neurologically normal brains and is believed typical of axonal as opposed to dendritic SBs.

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Zhu, Xiaodong, Yang Liu, Yanqing Yin, Aiyun Shao, Bo Zhang, Sunghoon Kim, and Jiawei Zhou. "MSC p43 required for axonal development in motor neurons." Proceedings of the National Academy of Sciences 106, no. 37 (August 26, 2009): 15944–49. http://dx.doi.org/10.1073/pnas.0901872106.

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Neuron connectivity and correct neural function largely depend on axonal integrity. Neurofilaments (NFs) constitute the main cytoskeletal network maintaining the structural integrity of neurons and exhibit dynamic changes during axonal and dendritic growth. However, the mechanisms underlying axonal development and maintenance remain poorly understood. Here, we identify that multisynthetase complex p43 (MSC p43) is essential for NF assembly and axon maintenance. The MSC p43 protein was predominantly expressed in central neurons and interacted with NF light subunit in vivo. Mice lacking MSC p43 exhibited axon degeneration in motor neurons, defective neuromuscular junctions, muscular atrophy, and motor dysfunction. Furthermore, MSC p43 depletion in mice caused disorganization of the axonal NF network. Mechanistically, MSC p43 is required for maintaining normal phosphorylation levels of NFs. Thus, MSC p43 is indispensable in maintaining axonal integrity. Its dysfunction may underlie the NF disorganization and axon degeneration associated with motor neuron degenerative diseases.

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Linden, Rafael. "Dendritic competition in the developing retina: Ganglion cell density gradients and laterally displaced dendrites." Visual Neuroscience 10, no. 2 (March 1993): 313–24. http://dx.doi.org/10.1017/s0952523800003710.

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AbstractDendrites of retinal ganglion cells (RGCs) tend to be distributed preferentially toward areas of reduced RGC density. This, however, does not occur in the retina of normal pigmented rats, in which it has been suggested that the centro-peripheral gradient of RGC density is too shallow to provide directional guidance to growing dendrites. In this study, laterally displaced dendrites of RGCs retrogradely labeled with horseradish peroxidase were related to cell density gradients induced experimentally in the rat retina. Neonatal unilateral lesions of the optic tract produced retrograde degeneration of contralaterally projecting RGCs, but spared ipsilaterally projecting neurons in the same retina. These lesions created an anomalous temporal to nasal gradient of cell density across the decussation line, opposite to the nasal to temporal gradient found along the same axis in either normal rats or rats that had the contralateral eye removed at birth. RGCs in rats that received optic tract lesions had their dendrites displaced laterally toward the depleted nasal retina, while in either normal or enucleated rats there was no naso-temporal asymmetry. The lateral displacement affected both primary dendrites and higher-order branches. However, the gradient of cell density after optic tract lesions was less steep than the gradient in either normal or enucleated rats. To test for the presence of steeper gradients at early stages of development, RGC density gradients were also examined at postnatal day 5 (P5). In normal rats, the RGCs were homogeneously distributed throughout the retina, while rats given optic tract lesions at birth already showed a temporo-nasal density gradient at P5. Still, this anomalous gradient was less steep than that found in normal adults. It is concluded that the time course, rather than the steepness of the RGC density gradient, is the major determinant of the lateral displacement of dendritic arbors with respect to the soma in developing RGCs. The data are consistent with the idea that the overall shape of dendritic arbors depends in part on dendritic competition during retinal development.

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Dent, Erik W. "Of microtubules and memory: implications for microtubule dynamics in dendrites and spines." Molecular Biology of the Cell 28, no. 1 (January 2017): 1–8. http://dx.doi.org/10.1091/mbc.e15-11-0769.

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Microtubules (MTs) are cytoskeletal polymers composed of repeating subunits of tubulin that are ubiquitously expressed in eukaryotic cells. They undergo a stochastic process of polymerization and depolymerization from their plus ends termed dynamic instability. MT dynamics is an ongoing process in all cell types and has been the target for the development of several useful anticancer drugs, which compromise rapidly dividing cells. Recent studies also suggest that MT dynamics may be particularly important in neurons, which develop a highly polarized morphology, consisting of a single axon and multiple dendrites that persist throughout adulthood. MTs are especially dynamic in dendrites and have recently been shown to polymerize directly into dendritic spines, the postsynaptic compartment of excitatory neurons in the CNS. These transient polymerization events into dendritic spines have been demonstrated to play important roles in synaptic plasticity in cultured neurons. Recent studies also suggest that MT dynamics in the adult brain function in the essential process of learning and memory and may be compromised in degenerative diseases, such as Alzheimer’s disease. This raises the possibility of targeting MT dynamics in the design of new therapeutic agents.

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Hamori, J. "Morphological plasticity of postsynaptic neurones in reactive synaptogenesis." Journal of Experimental Biology 153, no. 1 (October 1, 1990): 251–60. http://dx.doi.org/10.1242/jeb.153.1.251.

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Partial deafferentation of certain brain regions (septal nuclei, hippocampus, etc.) in adult animals results (1) in the disappearance of degenerating axon terminals and (2) in the short-term persistence of vacant postsynaptic sites. These postsynaptic sites have been shown to be re-supplied by sprouted axon terminals of intact axons. This paper will demonstrate that, in brain regions (e.g. cerebellar cortex, lateral geniculate nucleus) where axonal sprouting of local elements or of persisting afferent axons is negligible or absent, synaptic reorganization involves the active participation of postsynaptic dendritic and somatic elements of surviving local nerve cells. Synaptic regeneration can be demonstrated by morphological means both in developing and in adult central nervous system. The dendrites may show two types of response to deafferentation: (1) the formation of presynaptic specializations along their otherwise ‘classical’ postsynaptic membrane (the axonization of dendrites) resulting in the formation of new, dendrodendritic synapses, and (2) the ‘adaptive’ (structural) reduction in size (‘atrophy’) of the denervated nerve cell dendritic arborization, leading to a relative increase in density of the surviving (though non-sprouting) afferent axon terminals. In both cases a partial functional recovery can be demonstrated.

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Caliaperumal, Jayalakshmi, Sonia Brodie, Yonglie Ma, and Frederick Colbourne. "Thrombin Causes Neuronal Atrophy and Acute but not Chronic Cell Death." Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 41, no. 6 (November 2014): 714–20. http://dx.doi.org/10.1017/cjn.2014.105.

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AbstractBackground: Brain injury after intracerebral hemorrhage (ICH) arises from numerous contributors, of which some also play essential roles. Notably, thrombin production, needed to stop bleeding, also causes acute cell death and edema. In some rodent models of ICH, peri-hematoma neurons die over weeks. Hence we evaluated whether thrombin is responsible for this chronic degeneration. Functional impairments after ICH also result from sub-lethal damage to neurons, especially the loss of dendrites. Thus, we evaluated whether thrombin infusion alone, a reductionist model of ICH, causes similar injury. Methods: Adult rats had a modest intra-striatal infusion of thrombin (1 U) or saline followed by a behavioral test, to verify impairment, 7 days later. After this they were euthanized and tissue stained with Golgi-Cox solution to allow the assessment of dendritic morphology in striatal neurons. In a second experiment, rats survived 7 or 60 days after thrombin infusion in order to histologically determine lesion volume. Results: Thrombin caused early cell death and considerable atrophy in surviving peri-lesion neurons, which had less than half of their usual numbers of branches. However, total tissue loss was comparable at 7 (24.1 mm3) and 60 days (25.6 mm3). Conclusion: Thrombin infusion causes early cell death and neuronal atrophy in nearby surviving striatal neurons but thrombin does not cause chronic tissue loss. Thus, the chronic degeneration found after ICH in rats is not simply and solely due to acute thrombin production. Nonetheless, thrombin is an important contributor to behavioral dysfunction because it causes cell death and substantial dendritic injury.

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Yang, Yi, Michael Coleman, Lihui Zhang, Xiaoxiang Zheng, and Zhenyu Yue. "Autophagy in axonal and dendritic degeneration." Trends in Neurosciences 36, no. 7 (July 2013): 418–28. http://dx.doi.org/10.1016/j.tins.2013.04.001.

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Qi, Xin. "eIF2α links mitochondrial dysfunction to dendritic degeneration." Journal of Cell Biology 216, no. 3 (February 16, 2017): 555–57. http://dx.doi.org/10.1083/jcb.201701062.

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Although mitochondrial dysfunction has been associated with dendritic pathology in many neuronal types, how mitochondrial impairment causes the vulnerability of neuronal subtypes remains unknown. In this issue, Tsuyama et al. (2017. J. Cell Biol. https://doi.org/10.1083/jcb.201604065) identify eIF2α phosphorylation as a critical regulator of mitochondrial dysfunction-mediated selective dendritic loss in Drosophila neurons.

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MIZE, R. RANNEY, and GRACE D. BUTLER. "The NMDAR1 subunit of the N-methyl-D-aspartate receptor is localized at postsynaptic sites opposite both retinal and cortical terminals in the cat superior colliculus." Visual Neuroscience 17, no. 1 (January 2000): 41–53. http://dx.doi.org/10.1017/s0952523800171044.

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The N-methyl-D-aspartate receptor (NMDAR) is an ionotropic glutamate receptor that is important in neurotransmission as well as in processes of synaptic plasticity in the mammalian superior colliculus (SC). Despite the importance of this receptor in synaptic transmission, there is as yet no evidence that demonstrates directly the synaptic localization of the NMDAR receptor in SC. We have used electron-microscope (EM) immunocytochemistry to localize the NMDAR1 subunit of this receptor protein and its association with sensory afferents in the cat SC. Retinal synaptic terminals were identified by normal morphology and cortical synaptic terminals by degeneration after lesions of areas 17–18 of the visual cortex. At the light-microscope level, label was densest within the superficial gray and upper optic layers, but also present in all other layers. Label was contained within cell bodies, dendrites, and a few putative axons. At the EM level, antibody labeling was found along postsynaptic densifications and internalized within the cytoplasm of a variety of dendrites and some cell bodies. Postsynaptic profiles labeled by NMDAR1 included conventional dendrites and presynaptic dendrites which contained pleomorphic synaptic vesicles and are known to be GABAergic. Many of the labeled postsynaptic densifications of both of these profile types received synaptic inputs from retinal or cortical terminals. Virtually no NMDAR1 immunoreactivity was found on thin dendritic thorns or putative spines, even when these were postsynaptic to retinal or cortical terminals. In summary, these results show that the NMDAR1 subunit is postsynaptic to both retinal and cortical afferents, which are known to be glutamatergic, and are consistent with physiological evidence showing that stimulation of either pathway can activate the NMDA receptor.

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Kanjhan, Refik, Peter G. Noakes, and Mark C. Bellingham. "Emerging Roles of Filopodia and Dendritic Spines in Motoneuron Plasticity during Development and Disease." Neural Plasticity 2016 (2016): 1–31. http://dx.doi.org/10.1155/2016/3423267.

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Motoneurons develop extensive dendritic trees for receiving excitatory and inhibitory synaptic inputs to perform a variety of complex motor tasks. At birth, the somatodendritic domains of mouse hypoglossal and lumbar motoneurons have dense filopodia and spines. Consistent with Vaughn’s synaptotropic hypothesis, we propose a developmental unified-hybrid model implicating filopodia in motoneuron spinogenesis/synaptogenesis and dendritic growth and branching critical for circuit formation and synaptic plasticity at embryonic/prenatal/neonatal period. Filopodia density decreases and spine density initially increases until postnatal day 15 (P15) and then decreases by P30. Spine distribution shifts towards the distal dendrites, and spines become shorter (stubby), coinciding with decreases in frequency and increases in amplitude of excitatory postsynaptic currents with maturation. In transgenic mice, either overexpressing the mutated human Cu/Zn-superoxide dismutase (hSOD1G93A) gene or deficient in GABAergic/glycinergic synaptic transmission (gephyrin, GAD-67, or VGAT gene knockout), hypoglossal motoneurons develop excitatory glutamatergic synaptic hyperactivity. Functional synaptic hyperactivity is associated with increased dendritic growth, branching, and increased spine and filopodia density, involving actin-based cytoskeletal and structural remodelling. Energy-dependent ionic pumps that maintain intracellular sodium/calcium homeostasis are chronically challenged by activity and selectively overwhelmed by hyperactivity which eventually causes sustained membrane depolarization leading to excitotoxicity, activating microglia to phagocytose degenerating neurons under neuropathological conditions.

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Witzig, Victoria Sofie, Daniel Komnig, and Björn H. Falkenburger. "Changes in Striatal Medium Spiny Neuron Morphology Resulting from Dopamine Depletion Are Reversible." Cells 9, no. 11 (November 9, 2020): 2441. http://dx.doi.org/10.3390/cells9112441.

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The classical motor symptoms of Parkinson’s disease (PD) are caused by degeneration of dopaminergic neurons in the substantia nigra, which is followed by secondary dendritic pruning and spine loss at striatal medium spiny neurons (MSN). We hypothesize that these morphological changes at MSN underlie at least in part long-term motor complications in PD patients. In order to define the potential benefits and limitations of dopamine substitution, we tested in a mouse model whether dendritic pruning and spine loss can be reversible when dopaminergic axon terminals regenerate. In order to induce degeneration of nigrostriatal dopaminergic neurons we used the toxicity of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) in C57BL/6J mice; 30 mg/kg MPTP was applied i.p. on five consecutive days. In order to assess the consequences of dopamine depletion, mice were analyzed 21 days after the last injection. In order to test reversibility of MSN changes we exploited the property of this model that striatal axon terminals regenerate by sprouting within 90 days and analyzed a second cohort 90 days after MPTP. Degeneration of dopaminergic neurons was confirmed by counting TH-positive neurons in the substantia nigra and by analyzing striatal catecholamines. Striatal catecholamine recovered 90 days after MPTP. MSN morphology was visualized by Golgi staining and quantified as total dendritic length, number of dendritic branch points, and density of dendritic spines. All morphological parameters of striatal MSN were reduced 21 days after MPTP. Statistical analysis indicated that dendritic pruning and the reduction of spine density represent two distinct responses to dopamine depletion. Ninety days after MPTP, all morphological changes recovered. Our findings demonstrate that morphological changes in striatal MSN resulting from dopamine depletion are reversible. They suggest that under optimal conditions, symptomatic dopaminergic therapy might be able to prevent maladaptive plasticity and long-term motor complications in PD patients.

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Javier-Torrent, Míriam, and Carlos A. Saura. "Conventional and Non-Conventional Roles of Non-Muscle Myosin II-Actin in Neuronal Development and Degeneration." Cells 9, no. 9 (August 19, 2020): 1926. http://dx.doi.org/10.3390/cells9091926.

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Myosins are motor proteins that use chemical energy to produce mechanical forces driving actin cytoskeletal dynamics. In the brain, the conventional non-muscle myosin II (NMII) regulates actin filament cytoskeletal assembly and contractile forces during structural remodeling of axons and dendrites, contributing to morphology, polarization, and migration of neurons during brain development. NMII isoforms also participate in neurotransmission and synaptic plasticity by driving actin cytoskeletal dynamics during synaptic vesicle release and retrieval, and formation, maturation, and remodeling of dendritic spines. NMIIs are expressed differentially in cerebral non-neuronal cells, such as microglia, astrocytes, and endothelial cells, wherein they play key functions in inflammation, myelination, and repair. Besides major efforts to understand the physiological functions and regulatory mechanisms of NMIIs in the nervous system, their contributions to brain pathologies are still largely unclear. Nonetheless, genetic mutations or deregulation of NMII and its regulatory effectors are linked to autism, schizophrenia, intellectual disability, and neurodegeneration, indicating non-conventional roles of NMIIs in cellular mechanisms underlying neurodevelopmental and neurodegenerative disorders. Here, we summarize the emerging biological roles of NMIIs in the brain, and discuss how actomyosin signaling contributes to dysfunction of neurons and glial cells in the context of neurological disorders. This knowledge is relevant for a deep understanding of NMIIs on the pathogenesis and therapeutics of neuropsychiatric and neurodegenerative diseases.

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Zueva, M. V., A. N. Zhuravleva, and A. N. Bogolepova. "Dendritic Branching of Retinal Ganglion Cells as a Biomarker of Glaucomatous Optic Neuropathy and Alzheimer’s Disease and a Target of Neuroprotective Therapy." Ophthalmology in Russia 18, no. 2 (July 5, 2021): 198–207. http://dx.doi.org/10.18008/1816-5095-2021-2-198-207.

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Irreversible damage to the structure of axons and death of the retinal ganglion cell (RGC) soma in primary open-angle glaucoma (POAG) and Alzheimer’s disease (AD) develop against the background of the already existing clinical manifestation, which is preceded by a slow period of progressive loss of synapses and dendrites of the RGCs. Recent studies have shown that the integrity of the RGC’s dendritic branching can serve as both a target of neuroprotective therapy and a sensitive marker of retinal degeneration in AD and glaucoma. To develop methods of complex neuroprotective therapy, it is necessary to substantiate the targets and tactics of affecting the dendritic tree of the RGCs, the remodeling of which, according to modern concepts, can be closely and antagonistically related to the regeneration of the axon after its damage in trauma and neurodegenerative diseases. RGCs are highly capable of functional modification. Currently, it has been proven that the use of neuroprotective drugs and neurotrophins is promising for maintaining the adaptive plasticity of RGCs and restoring their synaptic contacts at the level of the retina and brain. Understanding the features of the adaptive plasticity of RGCs in AD and glaucoma will make possible to use technologies to activate the internal potential of neuronal remodeling, including the modification of dendritic branching of RGCs and regeneration of their axons, in the preclinical stages of these diseases. Increasing knowledge about the sequence and mechanisms of early events in the retina’s inner plexiform layer will contribute to the development of targeted neuroprotective therapy and new technologies to detect early POAG, AD, and, possibly, other systemic and local neurodegenerative conditions.

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Meghil, Mohamed M., and Christopher W. Cutler. "Oral Microbes and Mucosal Dendritic Cells, “Spark and Flame” of Local and Distant Inflammatory Diseases." International Journal of Molecular Sciences 21, no. 5 (February 28, 2020): 1643. http://dx.doi.org/10.3390/ijms21051643.

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Mucosal health and disease is mediated by a complex interplay between the microbiota (“spark”) and the inflammatory response (“flame”). Pathobionts, a specific class of microbes, exemplified by the oral microbe Porphyromonas gingivalis, live mostly “under the radar” in their human hosts, in a cooperative relationship with the indigenous microbiota. Dendritic cells (DCs), mucosal immune sentinels, often remain undisturbed by such microbes and do not alert adaptive immunity to danger. At a certain tipping point of inflammation, an “awakening” of pathobionts occurs, wherein their active growth and virulence are stimulated, leading to a dysbiosis. Pathobiont becomes pathogen, and commensal becomes accessory pathogen. The local inflammatory outcome is the Th17-mediated degenerative bone disease, periodontitis (PD). In systemic circulation of PD subjects, inflammatory DCs expand, carrying an oral microbiome and promoting Treg and Th17 responses. At distant peripheral sites, comorbid diseases including atherosclerosis, Alzheimer’s disease, macular degeneration, chronic kidney disease, and others are reportedly induced. This review will review the immunobiology of DCs, examine the complex interplay of microbes and DCs in the pathogenesis of PD and its comorbid inflammatory diseases, and discuss the role of apoptosis and autophagy in this regard. Overall, the pathophysiological mechanisms of DC-mediated chronic inflammation and tissue destruction will be summarized.

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Journal articles on the topic 'Dendrite degeneration'

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