Synaptic transmission in the brain

1971 ◽  
Vol 49 (9) ◽  
pp. 519-523 ◽  
Author(s):  
K. Krnjević
Keyword(s):  
Synaptic Transmission ◽  
The Brain

scholarly journals Astroglial glutamate transporters in the brain: Regulating neurotransmitter homeostasis and synaptic transmission

2017 ◽  
Vol 95 (11) ◽  
pp. 2140-2151 ◽  
Author(s):  
Ciaran Murphy-Royal ◽  
Julien Dupuis ◽  
Laurent Groc ◽  
Stéphane H. R. Oliet
Keyword(s):  
Synaptic Transmission ◽  
Glutamate Transporters ◽  
The Brain

Synaptic Transmission with the Glia

Physiology ◽  
2001 ◽  
Vol 16 (4) ◽  
pp. 178-184 ◽  
Author(s):  
Sabino Vesce ◽  
Paola Bezzi ◽  
Andrea Volterra
Keyword(s):  
Synaptic Transmission ◽  
Glial Cells ◽  
Brain Function ◽  
Synaptic Integration ◽  
New Findings ◽  
The Brain

For decades, scientists thought that all of the missing secrets of brain function resided in neurons. However, a wave of new findings indicates that glial cells, formerly considered mere supporters and subordinate to neurons, participate actively in synaptic integration and processing of information in the brain.

scholarly journals Stochastic, structural and functional factors influencing AMPA and NMDA synaptic response variability: a review

2017 ◽  
Vol 1 (3) ◽  
Author(s):  
Vito Di Maio ◽  
Francesco Ventriglia ◽  
Silvia Santillo
Keyword(s):  
Nervous System ◽  
Synaptic Transmission ◽  
Learning And Memory ◽  
Information Transfer ◽  
Basic Mechanism ◽  
Response Variability ◽  
Synaptic Response ◽  
Factors Influencing ◽  
Functional Factors ◽  
The Brain

Synaptic transmission is the basic mechanism of information transfer between neurons not only in the brain, but along all the nervous system. In this review we will briefly summarize some of the main parameters that produce stochastic variability in the synaptic response. This variability produces different effects on important brain phenomena, like learning and memory, and, alterations of its basic factors can cause brain malfunctioning.

Early Defects of GABAergic Synapses in the Brain Stem of a MeCP2 Mouse Model of Rett Syndrome

2008 ◽  
Vol 99 (1) ◽  
pp. 112-121 ◽  
Author(s):  
L. Medrihan ◽  
E. Tantalaki ◽  
G. Aramuni ◽  
V. Sargsyan ◽  
I. Dudanova ◽  
...  
Keyword(s):  
Synaptic Transmission ◽  
Brain Stem ◽  
Rett Syndrome ◽  
Time Course ◽  
Molecular Mechanisms ◽  
Neurodevelopmental Disorder ◽  
Therapeutic Interventions ◽  
Ventrolateral Medulla ◽  
Diagnostic Tools ◽  
The Brain

Rett syndrome is a neurodevelopmental disorder caused by mutations in the transcriptional repressor methyl-CpG-binding protein 2 (MeCP2) and represents the leading genetic cause for mental retardation in girls. MeCP2-mutant mice have been generated to study the molecular mechanisms of the disease. It was suggested that an imbalance between excitatory and inhibitory neurotransmission is responsible for the behavioral abnormalities, although it remained largely unclear which synaptic components are affected and how cellular impairments relate to the time course of the disease. Here, we report that MeCP2 KO mice present an imbalance between inhibitory and excitatory synaptic transmission in the ventrolateral medulla already at postnatal day 7. Focusing on the inhibitory synaptic transmission we show that GABAergic, but not glycinergic, synaptic transmission is strongly depressed in MeCP2 KO mice. These alterations are presumably due to both decreased presynaptic γ-aminobutyric acid (GABA) release with reduced levels of the vesicular inhibitory transmitter transporter and reduced levels of postsynaptic GABAA-receptor subunits α2 and α4. Our data indicate that in the MeCP2 −/y mice specific synaptic molecules and signaling pathways are impaired in the brain stem during early postnatal development. These observations mandate the search for more refined diagnostic tools and may provide a rationale for the timing of future therapeutic interventions in Rett patients.

scholarly journals 14-3-3 Proteins in Glutamatergic Synapses

2018 ◽  
Vol 2018 ◽  
pp. 1-6 ◽  
Author(s):  
Jiajing Zhang ◽  
Yi Zhou
Keyword(s):  
Synaptic Transmission ◽  
Molecular Pathways ◽  
Glutamatergic Synapses ◽  
Synaptic Functions ◽  
The Future ◽  
Important Regulator ◽  
The Brain

The 14-3-3 proteins are a family of proteins that are highly expressed in the brain and particularly enriched at synapses. Evidence accumulated in the last two decades has implicated 14-3-3 proteins as an important regulator of synaptic transmission and plasticity. Here, we will review previous and more recent research that has helped us understand the roles of 14-3-3 proteins at glutamatergic synapses. A key challenge for the future is to delineate the 14-3-3-dependent molecular pathways involved in regulating synaptic functions.

Development and Regulation of Dendritic Spine Synapses

Physiology ◽  
2006 ◽  
Vol 21 (1) ◽  
pp. 38-47 ◽  
Author(s):  
Barbara Calabrese ◽  
Margaret S. Wilson ◽  
Shelley Halpain
Keyword(s):  
Synaptic Transmission ◽  
Dendritic Spines ◽  
Dendritic Spine ◽  
Excitatory Synapses ◽  
Dense Array ◽  
Complex Dynamic ◽  
Neuronal Dendrites ◽  
Spine Abnormalities ◽  
Dynamic Structures ◽  
The Brain

Dendritic spines are small protrusions from neuronal dendrites that form the postsynaptic component of most excitatory synapses in the brain. They play critical roles in synaptic transmission and plasticity. Recent advances in imaging and molecular technologies reveal that spines are complex, dynamic structures that contain a dense array of cytoskeletal, transmembrane, and scaffolding molecules. Several neurological and psychiatric disorders exhibit dendritic spine abnormalities.

Endocannabinoid-Mediated Control of Synaptic Transmission

2009 ◽  
Vol 89 (1) ◽  
pp. 309-380 ◽  
Author(s):  
Masanobu Kano ◽  
Takako Ohno-Shosaku ◽  
Yuki Hashimotodani ◽  
Motokazu Uchigashima ◽  
Masahiko Watanabe
Keyword(s):  
Synaptic Transmission ◽  
Intracellular Signaling ◽  
Cannabinoid Receptors ◽  
Endocannabinoid System ◽  
Brain Regions ◽  
New Era ◽  
Behavioral Studies ◽  
Electrophysiological Studies ◽  
The Brain ◽  
Subsequent Identification

The discovery of cannabinoid receptors and subsequent identification of their endogenous ligands (endocannabinoids) in early 1990s have greatly accelerated research on cannabinoid actions in the brain. Then, the discovery in 2001 that endocannabinoids mediate retrograde synaptic signaling has opened up a new era for cannabinoid research and also established a new concept how diffusible messengers modulate synaptic efficacy and neural activity. The last 7 years have witnessed remarkable advances in our understanding of the endocannabinoid system. It is now well accepted that endocannabinoids are released from postsynaptic neurons, activate presynaptic cannabinoid CB1 receptors, and cause transient and long-lasting reduction of neurotransmitter release. In this review, we aim to integrate our current understanding of functions of the endocannabinoid system, especially focusing on the control of synaptic transmission in the brain. We summarize recent electrophysiological studies carried out on synapses of various brain regions and discuss how synaptic transmission is regulated by endocannabinoid signaling. Then we refer to recent anatomical studies on subcellular distribution of the molecules involved in endocannabinoid signaling and discuss how these signaling molecules are arranged around synapses. In addition, we make a brief overview of studies on cannabinoid receptors and their intracellular signaling, biochemical studies on endocannabinoid metabolism, and behavioral studies on the roles of the endocannabinoid system in various aspects of neural functions.

scholarly journals The Mechanical Basis of Memory - the MeshCODE Theory

2020 ◽  
Author(s):  
Benjamin T. Goult
Keyword(s):  
Action Potential ◽  
Synaptic Transmission ◽  
Data Storage ◽  
Spike Trains ◽  
Binary Format ◽  
Potential Spike ◽  
Mechanical Basis ◽  
The Mind ◽  
And Storage ◽  
The Brain

The MeshCODE framework outlined here represents a unifying theory of data storage in animals, providing read/write storage of both dynamic and persistent information in a binary format. Mechanosensitive proteins, that contain force-dependent switches, can store information persistently which can be written/updated using small changes in mechanical force. These mechanosensitive proteins, such as talin, scaffold each and every synapse creating a meshwork of switches that forms a code, a MeshCODE. Synaptic transmission and action potential spike trains would operate the cytoskeletal machinery to write and update the synaptic MeshCODEs, propagating this coding throughout the brain and to the entire organism. Based on established biophysical principles, a mechanical basis for memory provides a physical location for data storage in the brain. Furthermore, the conversion and storage of sensory and temporal inputs into a binary format identifies an addressable read/write memory system supporting the view of the mind as an organic supercomputer.

scholarly journals Species-specific differences in synaptic transmission and plasticity

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Prateep Beed ◽  
Saikat Ray ◽  
Laura Moreno Velasquez ◽  
Alexander Stumpf ◽  
Daniel Parthier ◽  
...  
Keyword(s):  
Synaptic Plasticity ◽  
Synaptic Transmission ◽  
Mossy Fiber ◽  
Mossy Fibers ◽  
Evolutionary Divergence ◽  
Short Term Plasticity ◽  
Species Specific ◽  
The Brain ◽  
Lower Expression

Abstract Synaptic transmission and plasticity in the hippocampus are integral factors in learning and memory. While there has been intense investigation of these critical mechanisms in the brain of rodents, we lack a broader understanding of the generality of these processes across species. We investigated one of the smallest animals with conserved hippocampal macroanatomy—the Etruscan shrew, and found that while synaptic properties and plasticity in CA1 Schaffer collateral synapses were similar to mice, CA3 mossy fiber synapses showed striking differences in synaptic plasticity between shrews and mice. Shrew mossy fibers have lower long term plasticity compared to mice. Short term plasticity and the expression of a key protein involved in it, synaptotagmin 7 were also markedly lower at the mossy fibers in shrews than in mice. We also observed similar lower expression of synaptotagmin 7 in the mossy fibers of bats that are evolutionarily closer to shrews than mice. Species specific differences in synaptic plasticity and the key molecules regulating it, highlight the evolutionary divergence of neuronal circuit functions.

Astroglial contribution to tau-dependent neurodegeneration

2019 ◽  
Vol 476 (22) ◽  
pp. 3493-3504 ◽  
Author(s):  
Marta Sidoryk-Węgrzynowicz ◽  
Lidia Strużyńska
Keyword(s):  
Nervous System ◽  
Synaptic Transmission ◽  
Neurofibrillary Tangles ◽  
Neuronal Survival ◽  
Critical Role ◽  
Proper Function ◽  
Neuronal Dysfunction ◽  
Neuronal Function ◽  
Glutamate Homeostasis ◽  
The Brain

Astrocytes, by maintaining an optimal environment for neuronal function, play a critical role in proper function of mammalian nervous system. They regulate synaptic transmission and plasticity and protect neurons against toxic insults. Astrocytes and neurons interact actively via glutamine-glutamate cycle (GGC) that supports neuronal metabolic demands and neurotransmission. GGC deficiency may be involved in different diseases of the brain, where impaired astrocytic control of glutamate homeostasis contributes to neuronal dysfunction. This includes tau-dependent neurodegeneration, where astrocytes lose key molecules involved in regulation of glutamate/glutamine homeostasis, neuronal survival and synaptogenesis. Astrocytic dysfunction in tauopathy appears to precede neurodegeneration and overt tau neuropathology such as phosphorylation, aggregation and formation of neurofibrillary tangles. In this review, we summarize recent studies demonstrating that activation of astrocytes is strictly associated with neurodegenerative processes including those involved in tau related pathology. We propose that astrocytic dysfunction, by disrupting the proper neuron-glia signalling early in the disease, significantly contributes to tauopathy pathogenesis.

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