scholarly journals Environmental enrichment enhances precision and remodeling speed of synaptic nanoarchitecture revealed by crosstalk free two-color in vivo STED nanoscopy

2020 ◽  
Author(s):  
Waja Wegner ◽  
Heinz Steffens ◽  
Carola Gregor ◽  
Fred Wolf ◽  
Katrin I. Willig
Keyword(s):  
Synaptic Plasticity ◽  
Environmental Enrichment ◽  
Time Lapse ◽  
Functional Changes ◽  
Spine Head ◽  
Learning Capabilities ◽  
Brain Circuitry ◽  
Time Lapse Imaging ◽  
Enhanced Learning

AbstractSynaptic plasticity underlies long-lasting structural and functional changes to brain circuitry and its experience-dependent remodeling can be fundamentally enhanced by environmental enrichment. It is unknown, however, whether and how environmental enrichment alters the morphology and dynamics of individual synapses. Here, we present a virtually crosstalk free, two-color in vivo STED microscope to simultaneously superresolve the dynamics of the postsynaptic density protein PSD95 and spine geometry. With environmental enrichment, the size distribution of PSD95 and spine head sizes were narrower than in controls, indicating that synaptic strength is set more precisely with environmental enrichment. Spine head geometry and PSD95 assemblies were highly dynamic exhibiting multiplicative size changes. With environmental enrichment, the topography of PSD95 nanoorganization was more dynamic and the magnitude of reorganization increased systematically with time. Thus, two-color in vivo time-lapse imaging of synaptic nanoorganization uncovers a unique synaptic nanodynamics associated with the enhanced learning capabilities under environmental enrichment.

Topical Review: Neuronal Migration in Cortical Development

2004 ◽  
Vol 19 (3) ◽  
pp. 274-279
Author(s):  
Shigeaki Kanatani ◽  
Hidenori Tabata ◽  
Kazunori Nakajima
Keyword(s):  
Neuronal Migration ◽  
Radial Glia ◽  
Asymmetric Cell Division ◽  
Time Lapse ◽  
Radial Glial Cells ◽  
Daughter Cells ◽  
Radial Glial ◽  
Time Lapse Imaging ◽  
Mitotic Behavior

Cortical formation in the developing brain is a highly complicated process involving neuronal production (through symmetric or asymmetric cell division) interaction of radial glia with neuronal migration, and multiple modes of neuronal migration. It has been convincingly demonstrated by numerous studies that radial glial cells are neural stem cells. However, the processes by which neurons arise from radial glia and migrate to their final destinations in vivo are not yet fully understood. Recent studies using time-lapse imaging of neuronal migration are giving investigators an increasingly more detailed understanding of the mitotic behavior of radial glia and the migrating behavior of their daughter cells. In this review, we describe recent progress in elucidating neuronal migration in brain formation and how neuronal migration is disturbed by mutations in genes that control this process. ( J Child Neurol 2005;20:274—279).

scholarly journals Individual neuronal subtypes control initial myelin sheath growth and stabilization

2020 ◽  
Vol 15 (1) ◽  
Author(s):  
Heather N. Nelson ◽  
Anthony J. Treichel ◽  
Erin N. Eggum ◽  
Madeline R. Martell ◽  
Amanda J. Kaiser ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Central Nervous System ◽  
Nervous System ◽  
Myelin Sheath ◽  
Time Lapse ◽  
Marked Individual ◽  
Larval Zebrafish ◽  
Sheath Formation ◽  
Time Lapse Imaging

Abstract Background In the developing central nervous system, pre-myelinating oligodendrocytes sample candidate nerve axons by extending and retracting process extensions. Some contacts stabilize, leading to the initiation of axon wrapping, nascent myelin sheath formation, concentric wrapping and sheath elongation, and sheath stabilization or pruning by oligodendrocytes. Although axonal signals influence the overall process of myelination, the precise oligodendrocyte behaviors that require signaling from axons are not completely understood. In this study, we investigated whether oligodendrocyte behaviors during the early events of myelination are mediated by an oligodendrocyte-intrinsic myelination program or are over-ridden by axonal factors. Methods To address this, we utilized in vivo time-lapse imaging in embryonic and larval zebrafish spinal cord during the initial hours and days of axon wrapping and myelination. Transgenic reporter lines marked individual axon subtypes or oligodendrocyte membranes. Results In the larval zebrafish spinal cord, individual axon subtypes supported distinct nascent sheath growth rates and stabilization frequencies. Oligodendrocytes ensheathed individual axon subtypes at different rates during a two-day period after initial axon wrapping. When descending reticulospinal axons were ablated, local spinal axons supported a constant ensheathment rate despite the increased ratio of oligodendrocytes to target axons. Conclusion We conclude that properties of individual axon subtypes instruct oligodendrocyte behaviors during initial stages of myelination by differentially controlling nascent sheath growth and stabilization.

In Vivo Time-Lapse Imaging of Neuronal Development inXenopus

2013 ◽  
Vol 2013 (9) ◽  
pp. pdb.top077156 ◽  
Author(s):  
Edward S. Ruthazer ◽  
Anne Schohl ◽  
Neil Schwartz ◽  
Aydin Tavakoli ◽  
Marc Tremblay ◽  
...  
Keyword(s):  
Neuronal Development ◽  
Time Lapse ◽  
Time Lapse Imaging

scholarly journals Sindbis Virus-Induced Neuronal Death Is both Necrotic and Apoptotic and Is Ameliorated byN-Methyl-d-Aspartate Receptor Antagonists

2001 ◽  
Vol 75 (15) ◽  
pp. 7114-7121 ◽  
Author(s):  
Jennifer L. Nargi-Aizenman ◽  
Diane E. Griffin
Keyword(s):  
Cell Death ◽  
Cortical Neurons ◽  
Sindbis Virus ◽  
Apoptotic Cell ◽  
Time Lapse ◽  
Apoptotic Cell Death ◽  
Time Lapse Imaging ◽  
Alphavirus Infection

ABSTRACT Virus infection of neurons leads to different outcomes ranging from latent and noncytolytic infection to cell death. Viruses kill neurons directly by inducing either apoptosis or necrosis or indirectly as a result of the host immune response. Sindbis virus (SV) is an alphavirus that induces apoptotic cell death both in vitro and in vivo. However, apoptotic changes are not always evident in neurons induced to die by alphavirus infection. Time lapse imaging revealed that SV-infected primary cortical neurons exhibited both apoptotic and necrotic morphological features and that uninfected neurons in the cultures also died. Antagonists of the N-methyl-d-aspartate (NMDA) subtype of glutamate receptors protected neurons from SV-induced death without affecting virus replication or SV-induced apoptotic cell death. These results provide evidence that SV infection activates neurotoxic pathways that result in aberrant NMDA receptor stimulation and damage to infected and uninfected neurons.

scholarly journals In vivo Postnatal Electroporation and Time-lapse Imaging of Neuroblast Migration in Mouse Acute Brain Slices

10.3791/50905 ◽  
2013 ◽  
Author(s):  
Martina Sonego ◽  
Ya Zhou ◽  
Madeleine Julie Oudin ◽  
Patrick Doherty ◽  
Giovanna Lalli
Keyword(s):  
Brain Slices ◽  
Time Lapse ◽  
Neuroblast Migration ◽  
Time Lapse Imaging

In vivo time-lapse imaging of mitochondria in healthy and diseased peripheral myelin sheath

Mitochondrion ◽  
2015 ◽  
Vol 23 ◽  
pp. 32-41 ◽  
Author(s):  
Sergio Gonzalez ◽  
Ruani Fernando ◽  
Jade Berthelot ◽  
Claire Perrin-Tricaud ◽  
Emmanuelle Sarzi ◽  
...  
Keyword(s):  
Myelin Sheath ◽  
Time Lapse ◽  
Time Lapse Imaging

scholarly journals Long-term in vivo time-lapse imaging of synapse development and plasticity in the cerebellum

2014 ◽  
Vol 111 (1) ◽  
pp. 208-216 ◽  
Author(s):  
Naoko Nishiyama ◽  
Jeremy Colonna ◽  
Elise Shen ◽  
Jennifer Carrillo ◽  
Hiroshi Nishiyama
Keyword(s):  
In Vivo Imaging ◽  
Time Window ◽  
Time Lapse ◽  
Mammalian Brain ◽  
Cerebellar Neurons ◽  
Brain Functions ◽  
Time Lapse Imaging ◽  
Synaptic Circuitry

Synapses are continuously formed and eliminated throughout life in the mammalian brain, and emerging evidence suggests that this structural plasticity underlies experience-dependent changes of brain functions such as learning and long-term memory formation. However, it is generally difficult to understand how the rewiring of synaptic circuitry observed in vivo eventually relates to changes in animal's behavior. This is because afferent/efferent connections and local synaptic circuitries are very complicated in most brain regions, hence it is largely unclear how sensorimotor information is conveyed, integrated, and processed through a brain region that is imaged. The cerebellar cortex provides a particularly useful model to challenge this problem because of its simple and well-defined synaptic circuitry. However, owing to the technical difficulty of chronic in vivo imaging in the cerebellum, it remains unclear how cerebellar neurons dynamically change their structures over a long period of time. Here, we showed that the commonly used method for neocortical in vivo imaging was not ideal for long-term imaging of cerebellar neurons, but simple optimization of the procedure significantly improved the success rate and the maximum time window of chronic imaging. The optimized method can be used in both neonatal and adult mice and allows time-lapse imaging of cerebellar neurons for more than 5 mo in ∼80% of animals. This method allows vital observation of dynamic cellular processes such as developmental refinement of synaptic circuitry as well as long-term changes of neuronal structures in adult cerebellum under longitudinal behavioral manipulations.

scholarly journals Cytoplasmic dynamics of myosin IIA and IIB: spatial ‘sorting’ of isoforms in locomoting cells

1998 ◽  
Vol 111 (15) ◽  
pp. 2085-2095 ◽  
Author(s):  
J. Kolega
Keyword(s):  
Cultured Cells ◽  
Myosin Ii ◽  
Cell Movement ◽  
Leading Edge ◽  
Time Lapse ◽  
Living Cells ◽  
Immunofluorescence Staining ◽  
Spatial Sorting ◽  
Time Lapse Imaging

Different isoforms of non-muscle myosin II have different distributions in vivo, even within individual cells. In order to understand how these different distributions arise, the distribution and dynamics of non-muscle myosins IIA and myosin IIB were examined in cultured cells using immunofluorescence staining and time-lapse imaging of fluorescent analogs. Cultured bovine aortic endothelia contained both myosins IIA and IIB. Both isoforms distributed along stress fibers, in linear or punctate aggregates within lamellipodia, and diffusely around the nucleus. However, the A isoform was preferentially located toward the leading edge of migrating cells when compared with myosin IIB by double immunofluorescence staining. Conversely, the B isoform was enriched in structures at the cells' trailing edges. When fluorescent analogs of the two isoforms were co-injected into living cells, the injected myosins distributed with the same disparate localizations as endogenous myosins IIA and IIB. This indicated that the ability of the myosins to ‘sort’ within the cytoplasm is intrinsic to the proteins themselves, and not a result of localized synthesis or degradation. Furthermore, time-lapse imaging of injected analogs in living cells revealed differences in the rates at which the two isoforms rearranged during cell movement. The A isoform appeared in newly formed structures more rapidly than the B isoform, and was also lost more rapidly when structures disassembled. These observations suggest that the different localizations of myosins IIA and IIB reflect different rates at which the isoforms transit through assembly, movement and disassembly within the cell. The relative proportions of different myosin II isoforms within a particular cell type may determine the lifetimes of various myosin II-based structures in that cell.

scholarly journals Rapid disruption of the cortical microcirculation after mild traumatic brain injury

2019 ◽  
Author(s):  
Ellen D. Witkowski ◽  
Şefik Evren Erdener ◽  
Kıvılcım Kılıç ◽  
Sreekanth Kura ◽  
Jianbo Tang ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Vascular Dysfunction ◽  
Metabolic Stress ◽  
Time Lapse ◽  
Post Injury ◽  
Injury Model ◽  
Time Lapse Imaging

AbstractTraumatic brain injury (TBI) is a major source of cognitive deficits affecting millions annually. The bulk of human injuries are mild, causing little or no macroscopic damage to neural tissue, yet can still lead to long-term neuropathology manifesting months or years later. Although the cellular stressors that ultimately lead to chronic pathology are poorly defined, one notable candidate is metabolic stress due to reduced cerebral blood flow (CBF), which is common to many forms of TBI. Here we used high-resolution in vivo intracranial imaging in a rodent injury model to characterize deficits in the cortical microcirculation during both acute and chronic phases after mild TBI. We found that CBF dropped precipitously during immediate post-injury periods, decreasing to less than half of baseline levels within minutes and remaining suppressed for 1.5-2 hours. Repeated time-lapse imaging of the cortical microvasculature revealed further striking flow deficits in the capillary network, where 18% of vessels were completely occluded for extended periods after injury, and an additional >50% showed substantial stoppages. Decreased CBF was paralleled by extensive vasoconstriction that is likely to contribute to loss of flow. Our data indicate a major role for vascular dysfunction in even mild forms of TBI, and suggest that acute post-injury periods may be key therapeutic windows for interventions that restore flow and mitigate metabolic stress.

Sign in / Sign up

Export Citation Format

Share Document