scholarly journals The Emerging Role of Mechanics in Synapse Formation and Plasticity

2018 ◽  
Vol 12 ◽  
Author(s):  
Devrim Kilinc
Keyword(s):  
Synapse Formation

scholarly journals The intellectual disability gene Kirrel3 regulates target-specific mossy fiber synapse development in the hippocampus

eLife ◽  
2015 ◽  
Vol 4 ◽  
Author(s):  
E Anne Martin ◽  
Shruti Muralidhar ◽  
Zhirong Wang ◽  
Diégo Cordero Cervantes ◽  
Raunak Basu ◽  
...  
Keyword(s):  
Synapse Formation ◽  
Mossy Fiber ◽  
Neuron Activity ◽  
Target Cells ◽  
Synaptic Changes ◽  
Mossy Fiber Synapse ◽  
Ca3 Neurons ◽  
Circuit Function ◽  
Feed Forward Inhibition

Synaptic target specificity, whereby neurons make distinct types of synapses with different target cells, is critical for brain function, yet the mechanisms driving it are poorly understood. In this study, we demonstrate Kirrel3 regulates target-specific synapse formation at hippocampal mossy fiber (MF) synapses, which connect dentate granule (DG) neurons to both CA3 and GABAergic neurons. Here, we show Kirrel3 is required for formation of MF filopodia; the structures that give rise to DG-GABA synapses and that regulate feed-forward inhibition of CA3 neurons. Consequently, loss of Kirrel3 robustly increases CA3 neuron activity in developing mice. Alterations in the Kirrel3 gene are repeatedly associated with intellectual disabilities, but the role of Kirrel3 at synapses remained largely unknown. Our findings demonstrate that subtle synaptic changes during development impact circuit function and provide the first insight toward understanding the cellular basis of Kirrel3-dependent neurodevelopmental disorders.

scholarly journals Thrombospondins 1 and 2 are Necessary for Synaptic Plasticity and Functional Recovery after Stroke

2008 ◽  
Vol 28 (10) ◽  
pp. 1722-1732 ◽  
Author(s):  
Jason Liauw ◽  
Stanley Hoang ◽  
Michael Choi ◽  
Cagla Eroglu ◽  
Matthew Choi ◽  
...  
Keyword(s):  
Infarct Size ◽  
Functional Recovery ◽  
Synapse Formation ◽  
Axonal Sprouting ◽  
Wild Type ◽  
Synaptic Density ◽  
Significant Deficit ◽  
The Common ◽  
Distal Middle Cerebral Artery

Thrombospondins 1 and 2 (TSP-1/2) belong to a family of extracellular glycoproteins with angiostatic and synaptogenic properties. Although TSP-1/2 have been postulated to drive the resolution of postischemic angiogenesis, their role in synaptic and functional recovery is unknown. We investigated whether TSP-1/2 are necessary for synaptic and motor recovery after stroke. Focal ischemia was induced in 8- to 12-week-old wild-type (WT) and TSP-1/2 knockout (KO) mice by unilateral occlusion of the distal middle cerebral artery and the common carotid artery (CCA). Thrombospondins 1 and 2 increased after stroke, with both TSP-1 and TSP-2 colocalizing mostly to astrocytes. Wild-type and TSP-1/2 KO mice were compared in angiogenesis, synaptic density, axonal sprouting, infarct size, and functional recovery at different time points after stroke. Using the tongue protrusion test of motor function, we observed that TSP-1/2 KO mice exhibited significant deficit in their ability to recover function ( P < 0.05) compared with WT mice. No differences were found in infarct size and blood vessel density between the two groups after stroke. However, TSP-1/2 KO mice exhibited significant synaptic density and axonal sprouting deficits. Deficiency of TSP-1/2 leads to impaired recovery after stroke mainly due to the role of these proteins in synapse formation and axonal outgrowth.

The role of support cells in the growth and differentiation of neurones in the abdominal ganglion of Aplysia

1981 ◽  
Vol 95 (1) ◽  
pp. 205-214
Author(s):  
S. M. Schacher
Keyword(s):  
Cell Body ◽  
Synapse Formation ◽  
Sea Water ◽  
Secretory Granules ◽  
Body Growth ◽  
Abdominal Ganglion ◽  
Morphological Properties ◽  
High Concentration ◽  
Premature Release

During the late premetamorphic stages of development, the abdominal ganglion of Aplysia is surrounded by a group of support cells which later develop morphological properties characteristic of glial cells. These support cells contain large secretory granules whose contents are released primarily after the onset of the metamorphic phase. The release of the granule contents may signal the burst of neuronal growth and maturation that occurs following metamorphosis. The evidence supporting this idea is the following: (1) The release of the granule material after the onset of metamorphosis coincides with an increase in cell body growth and a more marked increase in the density of synapses within the neuropil. Both release and neuronal maturation can be blocked when metamorphosis is postponed by withholding the appropriate macroalgal substrate. (2) Premature release of the granule contents 2-3 weeks before metamorphosis with artificial sea water containing a high concentration of potassium results in an increase in cell body growth, density of synapses, and the number of spines formed and contacts received by specific identified cells. (3) Artificially inducing the release of the granule material in animals whose metamorphosis has been prevented (by withholding the appropriate substrate) still produces an increase in cell body growth and density of synapses. These results suggest that the release of material from support cell granules provides a general stimulus for neuronal differentiation including cell body growth, spine development, and synapse formation.

scholarly journals MicroRNAs in brain development and cerebrovascular pathophysiology

2019 ◽  
Vol 317 (1) ◽  
pp. C3-C19 ◽  
Author(s):  
Qingyi Ma ◽  
Lubo Zhang ◽  
William J. Pearce
Keyword(s):  
Brain Development ◽  
Synapse Formation ◽  
Current Knowledge ◽  
Great Promise ◽  
Ischemic Brain ◽  
Neural Lineage ◽  
Cell Proliferation And Differentiation ◽  
Proliferation And Differentiation ◽  
And Function

MicroRNAs (miRNAs) are a class of highly conserved non-coding RNAs with 21–25 nucleotides in length and play an important role in regulating gene expression at the posttranscriptional level via base-paring with complementary sequences of the 3′-untranslated region of the target gene mRNA, leading to either transcript degradation or translation inhibition. Brain-enriched miRNAs act as versatile regulators of brain development and function, including neural lineage and subtype determination, neurogenesis, synapse formation and plasticity, neural stem cell proliferation and differentiation, and responses to insults. Herein, we summarize the current knowledge regarding the role of miRNAs in brain development and cerebrovascular pathophysiology. We review recent progress of the miRNA-based mechanisms in neuronal and cerebrovascular development as well as their role in hypoxic-ischemic brain injury. These findings hold great promise, not just for deeper understanding of basic brain biology but also for building new therapeutic strategies for prevention and treatment of pathologies such as cerebral ischemia.

scholarly journals Right Place at the Right Time: How Changes in Protocadherins Affect Synaptic Connections Contributing to the Etiology of Neurodevelopmental Disorders

Cells ◽  
2020 ◽  
Vol 9 (12) ◽  
pp. 2711
Author(s):  
Maria Mancini ◽  
Silvia Bassani ◽  
Maria Passafaro
Keyword(s):  
Cell Adhesion ◽  
Neurodevelopmental Disorders ◽  
Synapse Formation ◽  
Large Fraction ◽  
Critical Role ◽  
Basic Research ◽  
Axon Pathfinding ◽  
Neurite Initiation ◽  
The Right

During brain development, neurons need to form the correct connections with one another in order to give rise to a functional neuronal circuitry. Mistakes during this process, leading to the formation of improper neuronal connectivity, can result in a number of brain abnormalities and impairments collectively referred to as neurodevelopmental disorders. Cell adhesion molecules (CAMs), present on the cell surface, take part in the neurodevelopmental process regulating migration and recognition of specific cells to form functional neuronal assemblies. Among CAMs, the members of the protocadherin (PCDH) group stand out because they are involved in cell adhesion, neurite initiation and outgrowth, axon pathfinding and fasciculation, and synapse formation and stabilization. Given the critical role of these macromolecules in the major neurodevelopmental processes, it is not surprising that clinical and basic research in the past two decades has identified several PCDH genes as responsible for a large fraction of neurodevelopmental disorders. In the present article, we review these findings with a focus on the non-clustered PCDH sub-group, discussing the proteins implicated in the main neurodevelopmental disorders.

scholarly journals PUFA and their derivatives in neurotransmission and synapses: a new hallmark of synaptopathies

2020 ◽  
Vol 79 (4) ◽  
pp. 388-403
Author(s):  
Mathieu Di Miceli ◽  
Clémentine Bosch-Bouju ◽  
Sophie Layé
Keyword(s):  
Synapse Formation ◽  
Synaptic Function ◽  
Past Century ◽  
High Concentration ◽  
Dietary Pufa ◽  
Synaptic Functions ◽  
Neuropsychiatric Diseases ◽  
Optimal Function ◽  
The Brain

PUFA of the n-3 and n-6 families are present in high concentration in the brain where they are major components of cell membranes. The main forms found in the brain are DHA (22 :6, n-3) and arachidonic acid (20:4, n-6). In the past century, several studies pinpointed that modifications of n-3 and n-6 PUFA levels in the brain through dietary supply or genetic means are linked to the alterations of synaptic function. Yet, synaptopathies emerge as a common characteristic of neurodevelopmental disorders, neuropsychiatric diseases and some neurodegenerative diseases. Understanding the mechanisms of action underlying the activity of PUFA at the level of synapses is thus of high interest. In this frame, dietary supplementation in PUFA aiming at restoring or promoting the optimal function of synapses appears as a promising strategy to treat synaptopathies. This paper reviews the link between dietary PUFA, synapse formation and the role of PUFA and their metabolites in synaptic functions.

scholarly journals The Role of MuSK in Synapse Formation and Neuromuscular Disease

2013 ◽  
Vol 5 (5) ◽  
pp. a009167-a009167 ◽  
Author(s):  
S. J. Burden ◽  
N. Yumoto ◽  
W. Zhang
Keyword(s):  
Neuromuscular Disease ◽  
Synapse Formation

scholarly journals DC-SIGN–mediated Infectious Synapse Formation Enhances X4 HIV-1 Transmission from Dendritic Cells to T Cells

2004 ◽  
Vol 200 (10) ◽  
pp. 1279-1288 ◽  
Author(s):  
Jean-François Arrighi ◽  
Marjorie Pion ◽  
Eduardo Garcia ◽  
Jean-Michel Escola ◽  
Yvette van Kooyk ◽  
...  
Keyword(s):  
T Cells ◽  
Dendritic Cells ◽  
T Cell ◽  
Hiv Infection ◽  
Cd4 T Cells ◽  
Synapse Formation ◽  
Model Systems ◽  
Hiv 1 ◽  
Infectious Synapse

Dendritic cells (DCs) are essential for the early events of human immunodeficiency virus (HIV) infection. Model systems of HIV sexual transmission have shown that DCs expressing the DC-specific C-type lectin DC-SIGN capture and internalize HIV at mucosal surfaces and efficiently transfer HIV to CD4+ T cells in lymph nodes, where viral replication occurs. Upon DC–T cell clustering, internalized HIV accumulates on the DC side at the contact zone (infectious synapse), between DCs and T cells, whereas HIV receptors and coreceptors are enriched on the T cell side. Viral concentration at the infectious synapse may explain, at least in part, why DC transmission of HIV to T cells is so efficient. Here, we have investigated the role of DC-SIGN on primary DCs in X4 HIV-1 capture and transmission using small interfering RNA–expressing lentiviral vectors to specifically knockdown DC-SIGN. We demonstrate that DC-SIGN− DCs internalize X4 HIV-1 as well as DC-SIGN+ DCs, although binding of virions is reduced. Strikingly, DC-SIGN knockdown in DCs selectively impairs infectious synapse formation between DCs and resting CD4+ T cells, but does not prevent the formation of DC–T cells conjugates. Our results demonstrate that DC-SIGN is required downstream from viral capture for the formation of the infectious synapse between DCs and T cells. These findings provide a novel explanation for the role of DC-SIGN in the transfer and enhancement of HIV infection from DCs to T cells, a crucial step for HIV transmission and pathogenesis.

Sign in / Sign up

Export Citation Format

Share Document