Endocannabinoids as Modulators of Synaptic Signaling

2009 ◽  
pp. 281-308 ◽  
Author(s):  
Sachin Patel ◽  
Cecilia J. Hillard
Keyword(s):  
Synaptic Signaling

scholarly journals Targeting of NF-κB to Dendritic Spines Is Required for Synaptic Signaling and Spine Development

2018 ◽  
Vol 38 (17) ◽  
pp. 4093-4103 ◽  
Author(s):  
Erica C. Dresselhaus ◽  
Matthew C.H. Boersma ◽  
Mollie K. Meffert
Keyword(s):  
Dendritic Spines ◽  
Synaptic Signaling ◽  
Spine Development

scholarly journals Proteomic insights into synaptic signaling in the brain: the past, present and future

2021 ◽  
Vol 14 (1) ◽  
Author(s):  
Yalan Xu ◽  
Xiuyue Song ◽  
Dong Wang ◽  
Yin Wang ◽  
Peifeng Li ◽  
...  
Keyword(s):  
Mass Spectrometry ◽  
Protein Complexes ◽  
Synaptic Signaling ◽  
Brain Functions ◽  
The Past ◽  
Data Independent Acquisition ◽  
Technological Advances ◽  
Neural Communication ◽  
Chemical Synapses ◽  
The Brain

AbstractChemical synapses in the brain connect neurons to form neural circuits, providing the structural and functional bases for neural communication. Disrupted synaptic signaling is closely related to a variety of neurological and psychiatric disorders. In the past two decades, proteomics has blossomed as a versatile tool in biological and biomedical research, rendering a wealth of information toward decoding the molecular machinery of life. There is enormous interest in employing proteomic approaches for the study of synapses, and substantial progress has been made. Here, we review the findings of proteomic studies of chemical synapses in the brain, with special attention paid to the key players in synaptic signaling, i.e., the synaptic protein complexes and their post-translational modifications. Looking toward the future, we discuss the technological advances in proteomics such as data-independent acquisition mass spectrometry (DIA-MS), cross-linking in combination with mass spectrometry (CXMS), and proximity proteomics, along with their potential to untangle the mystery of how the brain functions at the molecular level. Last but not least, we introduce the newly developed synaptomic methods. These methods and their successful applications marked the beginnings of the synaptomics era.

scholarly journals Notum coordinates synapse development via extracellular regulation of Wingless trans-synaptic signaling

Development ◽  
2017 ◽  
Vol 144 (19) ◽  
pp. 3499-3510 ◽  
Author(s):  
Danielle L. Kopke ◽  
Sofia C. Lima ◽  
Cyrille Alexandre ◽  
Kendal Broadie
Keyword(s):  
Synapse Development ◽  
Synaptic Signaling

scholarly journals The Effects of Hypoxia and Inflammation on Synaptic Signaling in the CNS

2016 ◽  
Vol 6 (1) ◽  
pp. 6 ◽  
Author(s):  
Gatambwa Mukandala ◽  
Ronan Tynan ◽  
Sinead Lanigan ◽  
John O’Connor
Keyword(s):  
Synaptic Signaling

scholarly journals Astroglial FMRP modulates synaptic signaling and behavior phenotypes in FXS mouse model

2020 ◽  
Author(s):  
Shan-Xue Jin ◽  
Haruki Higashimori ◽  
Christina Schin ◽  
Alessandra Tamashiro ◽  
Yuqin Men ◽  
...  
Keyword(s):  
Glutamate Uptake ◽  
Fragile X ◽  
Cell Types ◽  
Skill Learning ◽  
Spine Density ◽  
Novelty Preference ◽  
Synaptic Signaling ◽  
Selective Loss ◽  
State Duration ◽  
Cortical Hyperexcitability

AbstractFragile X syndrome (FXS) is one of the most common inherited intellectual disability (ID) disorders, in which the loss of FMRP protein induces a range of cellular signaling changes primarily through excess protein synthesis. Although neuron-centered molecular and cellular events underlying FXS have been characterized, how different CNS cell types are involved in typical FXS synaptic signaling changes and behavioral phenotypes is largely unknown. Recent evidence suggests that selective loss of astroglial FMRP is able to dysregulate glutamate uptake, increase spine density, and impair motor-skill learning. Here we investigated the effect of astroglial FMRP on synaptic signaling and FXS-related behavioral and learning phenotypes in astroglial Fmr1 cKO and cON mice in which FMRP expression is selectively diminished or restored in astroglia. We found that selective loss of astroglial FMRP contributes to cortical hyperexcitability by enhancing NMDAR-mediated evoked but not spontaneous miniEPSCs and elongating cortical UP state duration. Selective loss of astroglial FMRP is also sufficient to increase locomotor hyperactivity, significantly diminish social novelty preference, and induce memory acquisition and extinction deficits in astroglial Fmr1 cKO mice. Importantly, re-expression of astroglial FMRP is able to significantly rescue the hyperactivity (evoked NMDAR response, UP state duration, and open field test) and social novelty preference in astroglial Fmr1 cON mice. These results demonstrate a profound role of astroglial FMRP in the evoked synaptic signaling, spontaneously occurring cortical UP states, and FXS-related behavioral and learning phenotypes and provide important new insights in the cell type consideration for the FMRP reactivation strategy.

scholarly journals Synaptic Signaling by All-Trans Retinoic Acid in Homeostatic Synaptic Plasticity

Neuron ◽  
2008 ◽  
Vol 60 (2) ◽  
pp. 308-320 ◽  
Author(s):  
Jason Aoto ◽  
Christine I. Nam ◽  
Michael M. Poon ◽  
Pamela Ting ◽  
Lu Chen
Keyword(s):  
Retinoic Acid ◽  
Synaptic Plasticity ◽  
Synaptic Signaling ◽  
Homeostatic Synaptic Plasticity ◽  
Trans Retinoic Acid ◽  
All Trans Retinoic Acid
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