scholarly journals Neuronal Plasticity in the Juvenile and Adult Brain Regulated by the Extracellular Matrix

10.5772/62452 ◽  
2016 ◽  
Author(s):  
Max F.K. Happel ◽  
Renato Frischknecht
Keyword(s):  
Extracellular Matrix ◽  
Neuronal Plasticity ◽  
Adult Brain

scholarly journals Aggrecan Directs Extracellular Matrix-Mediated Neuronal Plasticity

2018 ◽  
Vol 38 (47) ◽  
pp. 10102-10113 ◽  
Author(s):  
Daire Rowlands ◽  
Kristian K. Lensjø ◽  
Tovy Dinh ◽  
Sujeong Yang ◽  
Melissa R. Andrews ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Neuronal Plasticity

scholarly journals Neurons, Glia, Extracellular Matrix and Neurovascular Unit: A Systems Biology Approach to the Complexity of Synaptic Plasticity in Health and Disease

2020 ◽  
Vol 21 (4) ◽  
pp. 1539 ◽  
Author(s):  
Ciro De Luca ◽  
Anna Maria Colangelo ◽  
Assunta Virtuoso ◽  
Lilia Alberghina ◽  
Michele Papa
Keyword(s):  
Extracellular Matrix ◽  
Synaptic Plasticity ◽  
Systems Biology ◽  
Synapse Formation ◽  
Neurovascular Unit ◽  
Synaptic Cleft ◽  
Adult Brain ◽  
Molecular Networks ◽  
Maladaptive Plasticity ◽  
Health And Disease

The synaptic cleft has been vastly investigated in the last decades, leading to a novel and fascinating model of the functional and structural modifications linked to synaptic transmission and brain processing. The classic neurocentric model encompassing the neuronal pre- and post-synaptic terminals partly explains the fine-tuned plastic modifications under both pathological and physiological circumstances. Recent experimental evidence has incontrovertibly added oligodendrocytes, astrocytes, and microglia as pivotal elements for synapse formation and remodeling (tripartite synapse) in both the developing and adult brain. Moreover, synaptic plasticity and its pathological counterpart (maladaptive plasticity) have shown a deep connection with other molecular elements of the extracellular matrix (ECM), once considered as a mere extracellular structural scaffold altogether with the cellular glue (i.e., glia). The ECM adds another level of complexity to the modern model of the synapse, particularly, for the long-term plasticity and circuit maintenance. This model, called tetrapartite synapse, can be further implemented by including the neurovascular unit (NVU) and the immune system. Although they were considered so far as tightly separated from the central nervous system (CNS) plasticity, at least in physiological conditions, recent evidence endorsed these elements as structural and paramount actors in synaptic plasticity. This scenario is, as far as speculations and evidence have shown, a consistent model for both adaptive and maladaptive plasticity. However, a comprehensive understanding of brain processes and circuitry complexity is still lacking. Here we propose that a better interpretation of the CNS complexity can be granted by a systems biology approach through the construction of predictive molecular models that enable to enlighten the regulatory logic of the complex molecular networks underlying brain function in health and disease, thus opening the way to more effective treatments.

scholarly journals 3D extracellular matrix microenvironment in bioengineered tissue models of primary pediatric and adult brain tumors

2019 ◽  
Vol 10 (1) ◽  
Author(s):  
Disha Sood ◽  
Min Tang-Schomer ◽  
Dimitra Pouli ◽  
Craig Mizzoni ◽  
Nicole Raia ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Brain Tumor ◽  
Brain Tumors ◽  
Adult Brain ◽  
Metabolic Imaging ◽  
Tumor Type ◽  
Label Free ◽  
Pediatric Ependymoma ◽  
Extracellular Lipid ◽  
Tumor Cell Behavior

Abstract Dynamic alterations in the unique brain extracellular matrix (ECM) are involved in malignant brain tumors. Yet studies of brain ECM roles in tumor cell behavior have been difficult due to lack of access to the human brain. We present a tunable 3D bioengineered brain tissue platform by integrating microenvironmental cues of native brain-derived ECMs and live imaging to systematically evaluate patient-derived brain tumor responses. Using pediatric ependymoma and adult glioblastoma as examples, the 3D brain ECM-containing microenvironment with a balance of cell-cell and cell-matrix interactions supports distinctive phenotypes associated with tumor type-specific and ECM-dependent patterns in the tumor cells’ transcriptomic and release profiles. Label-free metabolic imaging of the composite model structure identifies metabolically distinct sub-populations within a tumor type and captures extracellular lipid-containing droplets with potential implications in drug response. The versatile bioengineered 3D tumor tissue system sets the stage for mechanistic studies deciphering microenvironmental role in brain tumor progression.

scholarly journals Optical activation of TrkB neurotrophin receptor in mouse ventral hippocampus promotes plasticity and facilitates fear extinction

2021 ◽  
Author(s):  
Juzoh Umemori ◽  
Giuliano Didio ◽  
Frederike Winkel ◽  
Maria Llach Pou ◽  
Juliana Harkki ◽  
...  
Keyword(s):  
Neuronal Network ◽  
Neuronal Plasticity ◽  
Pyramidal Neurons ◽  
Light Exposure ◽  
Neuropsychiatric Symptoms ◽  
Ventral Hippocampus ◽  
Fear Extinction ◽  
Extinction Training ◽  
Adult Brain ◽  
Neurotrophin Receptor

AbstractSuccessful extinction of traumatic memories depends on neuronal plasticity in the fear extinction network. However, the mechanisms involved in the extinction process remain poorly understood. Here, we investigated the fear extinction network by using a new optogenetic technique that allows temporal and spatial control of neuronal plasticity in vivo. We optimized an optically inducible TrkB (CKII-optoTrkB), the receptor of the brain-derived neurotrophic factor, which can be activated upon blue light exposure to increase plasticity specifically in pyramidal neurons. The activation of CKII-optoTrkB facilitated the induction of LTP in Schaffer collateral-CA1 synapses after brief theta-burst stimulation and increased the expression of FosB in the pyramidal neurons of the ventral hippocampus, indicating enhanced plasticity in that brain area. We showed that optical stimulation of the CA1 region of the ventral hippocampus during fear extinction training led to an attenuated conditioned fear memory. This was a specific effect only observed when combining extinction training with CKII-optoTrkB activation, and not when using either intervention alone. Thus, TrkB activation in ventral CA1 pyramidal neurons promotes a state of neuronal plasticity that allows extinction training to guide neuronal network remodeling to overcome fear memories. Our methodology is a powerful tool to induce neuronal network remodeling in the adult brain, and can attenuate neuropsychiatric symptoms caused by malfunctioning networks.

scholarly journals The Chemorepulsive Protein Semaphorin 3A and Perineuronal Net-Mediated Plasticity

2016 ◽  
Vol 2016 ◽  
pp. 1-14 ◽  
Author(s):  
F. de Winter ◽  
J. C. F. Kwok ◽  
J. W. Fawcett ◽  
T. T. Vo ◽  
D. Carulli ◽  
...  
Keyword(s):  
Neural Plasticity ◽  
Neuronal Plasticity ◽  
Adult Brain ◽  
Critical Periods ◽  
Inhibitory Effects ◽  
Perineuronal Net ◽  
Neuronal Populations ◽  
Biochemical Interaction ◽  
Chondroitin Sulfate E ◽  
The Brain

During postnatal development, closure of critical periods coincides with the appearance of extracellular matrix structures, called perineuronal nets (PNN), around various neuronal populations throughout the brain. The absence or presence of PNN strongly correlates with neuronal plasticity. It is not clear how PNN regulate plasticity. The repulsive axon guidance proteins Semaphorin (Sema) 3A and Sema3B are also prominently expressed in the postnatal and adult brain. In the neocortex, Sema3A accumulates in the PNN that form around parvalbumin positive inhibitory interneurons during the closure of critical periods. Sema3A interacts with high-affinity with chondroitin sulfate E, a component of PNN. The localization of Sema3A in PNN and its inhibitory effects on developing neurites are intriguing features and may clarify how PNN mediate structural neural plasticity. In the cerebellum, enhanced neuronal plasticity as a result of an enriched environment correlates with reduced Sema3A expression in PNN. Here, we first review the distribution of Sema3A and Sema3B expression in the rat brain and the biochemical interaction of Sema3A with PNN. Subsequently, we review what is known so far about functional correlates of changes in Sema3A expression in PNN. Finally, we propose a model of how Semaphorins in the PNN may influence local connectivity.

Impact of the extracellular matrix on plasticity in juvenile and adult brains

e-Neuroforum ◽  
2016 ◽  
Vol 22 (1) ◽  
pp. 1-6 ◽  
Author(s):  
R. Frischknecht ◽  
Max F.K. Happel ◽  
Max F.K. Happel
Keyword(s):  
Extracellular Matrix ◽  
Therapeutic Potential ◽  
Adult Brain ◽  
Brain Maturation ◽  
Structural Stabilization ◽  
Vertebrate Brain ◽  
Flexible Adaptation ◽  
Complex Forms ◽  
Higher Cognitive Functions ◽  
Activity Dependent

AbstractIn the higher vertebrate brain, the delicate balance between structural stabilization and remodeling of synaptic networks changes over the life span. The juvenile brain is characterized by high structural plasticity. A critical step in brain maturation is the occurrence of the extracellular matrix (ECM) that structurally stabilizes neuronal tissue restricting the potential for neuronal remodeling and regeneration. Current research has only begun to understand how this putative limitation of adult neuronal plasticity might impact on learning-related plasticity, lifelong memory reformation and higher cognitive functions. In this review, we summarize recent evidence that recognizes the ECM and its activity- dependent modulation as a key regulator of learning-related plasticity in the adult brain. Experimental modulation of the ECM in local neuronal circuits further opens short-term windows of activity-dependent reorganization, promoting complex forms of cognitive flexible adaptation of valuable behavioral options. This further bears implications for guided neuroplasticity with regenerative and therapeutic potential.

scholarly journals Chondroitin Sulfate Induces Depression of Synaptic Transmission and Modulation of Neuronal Plasticity in Rat Hippocampal Slices

2015 ◽  
Vol 2015 ◽  
pp. 1-12 ◽  
Author(s):  
Elisa Albiñana ◽  
Javier Gutierrez-Luengo ◽  
Natalia Hernández-Juarez ◽  
Andrés M. Baraibar ◽  
Eulalia Montell ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Synaptic Transmission ◽  
Neuronal Plasticity ◽  
Chondroitin Sulphate ◽  
Hippocampal Slices ◽  
Long Term Potentiation ◽  
Dependent Manner ◽  
Perineuronal Net ◽  
Concentration Dependent Manner ◽  
Population Spike Amplitude

It is currently known that in CNS the extracellular matrix is involved in synaptic stabilization and limitation of synaptic plasticity. However, it has been reported that the treatment with chondroitinase following injury allows the formation of new synapses and increased plasticity and functional recovery. So, we hypothesize that some components of extracellular matrix may modulate synaptic transmission. To test this hypothesis we evaluated the effects of chondroitin sulphate (CS) on excitatory synaptic transmission, cellular excitability, and neuronal plasticity using extracellular recordings in the CA1 area of rat hippocampal slices. CS caused a reversible depression of evoked field excitatory postsynaptic potentials in a concentration-dependent manner. CS also reduced the population spike amplitude evoked after orthodromic stimulation but not when the population spikes were antidromically evoked; in this last case a potentiation was observed. CS also enhanced paired-pulse facilitation and long-term potentiation. Our study provides evidence that CS, a major component of the brain perineuronal net and extracellular matrix, has a function beyond the structural one, namely, the modulation of synaptic transmission and neuronal plasticity in the hippocampus.

scholarly journals Extracellular matrix supports excitation-inhibition balance in neuronal networks by stabilizing inhibitory synapses

2020 ◽  
Author(s):  
Egor Dzyubenko ◽  
Michael Fleischer ◽  
Daniel Manrique-Castano ◽  
Mina Borbor ◽  
Christoph Kleinschnitz ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Neuronal Network ◽  
Neuronal Plasticity ◽  
Neuronal Networks ◽  
Network Activity ◽  
Inhibitory Synapses ◽  
Neuronal Network Activity ◽  
The Brain

AbstractMaintaining the balance between excitation and inhibition is essential for the appropriate control of neuronal network activity. Sustained excitation-inhibition (E-I) balance relies on the orchestrated adjustment of synaptic strength, neuronal activity and network circuitry. While growing evidence indicates that extracellular matrix (ECM) of the brain is a crucial regulator of neuronal excitability and synaptic plasticity, it remains unclear whether and how ECM contributes to neuronal circuit stability. Here we demonstrate that the integrity of ECM supports the maintenance of E-I balance by retaining inhibitory connectivity. Depletion of ECM in mature neuronal networks preferentially decreases the density of inhibitory synapses and the size of individual inhibitory postsynaptic scaffolds. After ECM depletion, inhibitory synapse strength homeostatically increases via the reduction of presynaptic GABAB receptors. However, the inhibitory connectivity reduces to an extent that inhibitory synapse scaling is no longer efficient in controlling neuronal network activity. Our results indicate that the brain ECM preserves the balanced network state by stabilizing inhibitory synapses.Significance statementThe question how the brain’s extracellular matrix (ECM) controls neuronal plasticity and network activity is key for an appropriate understanding of brain functioning. In this study, we demonstrate that ECM depletion much more strongly affects the integrity of inhibitory than excitatory synapses in vitro and in vivo. We revealed that by retaining inhibitory connectivity, ECM ensures the efficiency of inhibitory control over neuronal network activity. Our work significantly expands our current state of knowledge about the mechanisms of neuronal network activity regulation. Our findings are similarly relevant for researchers working on the physiological regulation of neuronal plasticity in vitro and in vivo and for researchers studying the remodeling of neuronal networks upon brain injury, where prominent ECM alterations occur.

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