Silent glutamatergic synapses in the mammalian brain

1999 ◽  
Vol 77 (9) ◽  
pp. 735-737 ◽  
Author(s):  
John TR Isaac ◽  
Roger A Nicoll ◽  
Robert C Malenka
Keyword(s):  
Synaptic Plasticity ◽  
Nmda Receptors ◽  
Neural Activity ◽  
Long Term Potentiation ◽  
Mammalian Brain ◽  
Glutamatergic Synapses ◽  
Synaptic Localization ◽  
Term Potentiation ◽  
Ampa And Nmda Receptors

Excitatory synaptic transmission in the mammalian brain is mediated primarily by α-amino-3-hydroxy-5-methylisoxazolepropionic acid (AMPA) and N-methyl-D-aspartate (NMDA) receptors that are thought to be co-localized at individual synapses. However, recent electrophysiological and anatomical data suggest that the synaptic localization of AMPA and NMDA receptors may be independently regulated by neural activity. These data are reviewed here and the implications of these findings for the mechanisms underlying synaptic plasticity are discussed.Key words: glutamate receptor, long-term potentiation (LTP), synaptic plasticity, hippocampus, cortex.

scholarly journals GluR2 protein-protein interactions and the regulation of AMPA receptors during synaptic plasticity

2003 ◽  
Vol 358 (1432) ◽  
pp. 715-720 ◽  
Author(s):  
Fabrice Duprat ◽  
Michael Daw ◽  
Wonil Lim ◽  
Graham Collingridge ◽  
John Isaac
Keyword(s):  
Synaptic Plasticity ◽  
Ampa Receptor ◽  
Protein Interactions ◽  
Ampa Receptors ◽  
Long Term Potentiation ◽  
Synaptic Proteins ◽  
Mammalian Brain ◽  
Protein Protein Interactions ◽  
Term Potentiation

AMPA-type glutamate receptors mediate most fast excitatory synaptic transmissions in the mammalian brain. They are critically involved in the expression of long-term potentiation and long-term depression, forms of synaptic plasticity that are thought to underlie learning and memory. A number of synaptic proteins have been identified that interact with the intracellular C-termini of AMPA receptor subunits. Here, we review recent studies and present new experimental data on the roles of these interacting proteins in regulating the AMPA receptor function during basal synaptic transmission and plasticity.

scholarly journals Role of the Serotonin Receptor 7 in Brain Plasticity: From Development to Disease

2019 ◽  
Author(s):  
Marianna Crispino ◽  
Floriana Volpicelli ◽  
Carla Perrone-Capano
Keyword(s):  
Synaptic Plasticity ◽  
Serotonin Receptor ◽  
Brain Plasticity ◽  
Long Term Potentiation ◽  
Mammalian Brain ◽  
Receptor Subtype ◽  
Brain Physiology ◽  
Mature Brain ◽  
Term Potentiation

Our knowledge on the plastic functions of the serotonin (5-HT) receptor subtype 7 (5-HT7R) in the brain physiology and pathology considerably advanced in the last few years. A wealth of data show that the 5-HT7R is a key player in the establishment and remodeling of neuronal cytoarchitecture during development and in the mature brain, and its dysfunction is linked to neuropsychiatric and neurodevelopmental diseases. The involvement of this receptor in synaptic plasticity is further demonstrated by data showing that its activation allows to rescue long term potentiation (LTP) and long term depression (LTD) deficits in various animal models of neurodevelopmental diseases. In addition, it is becoming clear that the 5-HT7R is involved in inflammatory intestinal diseases, possibly playing a role in the gut-brain axis, and modulates the function of immune cells. In this review, we will mainly focus on recent findings on this receptor’s role in the structural and synaptic plasticity of the mammalian brain, although we will also illustrate novel aspects highlighted in gut and immune system.

scholarly journals Electro-acupuncture alleviates motor deficits and maladaptive striatal plasticity in partial-lesioned parkinsonian mice

2020 ◽  
Author(s):  
Wenting Su ◽  
Jianan Yu ◽  
Min Li ◽  
Ke Wang ◽  
Chang Liu ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Synaptic Plasticity ◽  
Nmda Receptors ◽  
Glutamate Receptors ◽  
Motor Skills ◽  
Ampa Receptors ◽  
Long Term Potentiation ◽  
Term Potentiation ◽  
6 Hydroxydopamine

Abstract Background Parkinson's disease is characterized by abnormal synaptic transmission in the corticostriatal circuit that leads to deficits in motor abilities. Electro-acupuncture has shown to improve the motor behaviors in parkinsonian models. However, the potential mechanisms underlying the electro-acupuncture treatment, specifically in the partial-lesioned model, remain unclear. Methods By utilizing multiple approaches, including electrophysiological, immunohistochemistrical, molecular and behavioral methods, we assessed the effect of electro-acupuncture on the motor dysfunction and striatal synaptic plasticity in a partial-lesioned mouse model induced by intrastriatal injection of 6-hydroxydopamine. Results Electro-acupuncture ameliorated the disrupted gross and fine motor skills in 6-hydroxydopamine-lesioned mice. Notably, electro-acupuncture not only restored the injured corticostriatal long-term potentiation, but also reversed the loss of GluN1-containing NMDA receptors and GluA1-containing AMPA receptors in the striatum. Furthermore, the antagonists selective for AMPA receptors and NMDA receptors blocked the effect of electro-acupuncture on the corticostriatal long-term potentiation in 6-hydroxydopamine-treated mice. Conclusions These data suggest that the postsynaptic glutamate receptors in the striatum undergo the maladaptive changes in the early stage of Parkinson's disease. Electro-acupuncture improves the motor skills via a mechanism involving the modulation of corticostriatal synaptic plasticity and specific glutamate receptors in a partial-lesioned rodent model.

scholarly journals In search of general mechanisms for long-lasting plasticity: Aplysia and the hippocampus

2003 ◽  
Vol 358 (1432) ◽  
pp. 757-763 ◽  
Author(s):  
Christopher Pittenger ◽  
Eric R. Kandel
Keyword(s):  
Synaptic Plasticity ◽  
Molecular Mechanisms ◽  
Long Term Potentiation ◽  
Mammalian Brain ◽  
Marine Snail ◽  
Synaptic Facilitation ◽  
Term Potentiation ◽  
Two Systems ◽  
Mechanisms Of Plasticity

Long-term synaptic plasticity is thought to underlie many forms of long-lasting memory. Long-lasting plasticity has been most extensively studied in the marine snail Aplysia and in the mammalian hippocampus, where Bliss and Lømo first described long-term potentiation 30 years ago. The molecular mechanisms of plasticity in these two systems have proven to have many similarities. Here, we briefly describe some of these areas of overlap. We then summarize recent advances in our understanding of the mechanisms of long-lasting synaptic facilitation in Aplysia and suggest that these may prove fruitful areas for future investigation in the mammalian hippocampus and at other synapses in the mammalian brain.

scholarly journals Differential Trafficking of AMPA and NMDA Receptors during Long-Term Potentiation in Awake Adult Animals

2007 ◽  
Vol 27 (51) ◽  
pp. 14171-14178 ◽  
Author(s):  
J. M. Williams ◽  
D. Guevremont ◽  
S. E. Mason-Parker ◽  
C. Luxmanan ◽  
W. P. Tate ◽  
...  
Keyword(s):  
Nmda Receptors ◽  
Long Term Potentiation ◽  
Term Potentiation ◽  
Ampa And Nmda Receptors

scholarly journals Role of the Serotonin Receptor 7 in Brain Plasticity: From Development to Disease

2020 ◽  
Vol 21 (2) ◽  
pp. 505 ◽  
Author(s):  
Marianna Crispino ◽  
Floriana Volpicelli ◽  
Carla Perrone-Capano
Keyword(s):  
Synaptic Plasticity ◽  
Serotonin Receptor ◽  
Brain Plasticity ◽  
Long Term Potentiation ◽  
Mammalian Brain ◽  
Receptor Subtype ◽  
Brain Physiology ◽  
Mature Brain ◽  
Term Potentiation

Our knowledge on the plastic functions of the serotonin (5-HT) receptor subtype 7 (5-HT7R) in the brain physiology and pathology have advanced considerably in recent years. A wealth of data show that 5-HT7R is a key player in the establishment and remodeling of neuronal cytoarchitecture during development and in the mature brain, and its dysfunction is linked to neuropsychiatric and neurodevelopmental diseases. The involvement of this receptor in synaptic plasticity is further demonstrated by data showing that its activation allows the rescue of long-term potentiation (LTP) and long-term depression (LTD) deficits in various animal models of neurodevelopmental diseases. In addition, it is becoming clear that the 5-HT7R is involved in inflammatory intestinal diseases, modulates the function of immune cells, and is likely to play a role in the gut-brain axis. In this review, we will mainly focus on recent findings on this receptor’s role in the structural and synaptic plasticity of the mammalian brain, although we will also illustrate novel aspects highlighted in gastrointestinal (GI) tract and immune system.

scholarly journals Long-Term Potentiation Induces Extrasynaptic Exocytosis of Glun2A-containing NMDA Receptors that is Mainly Controlled by SNAP23

2019 ◽  
Author(s):  
Xiaojun Yu ◽  
Wei Li ◽  
Tong Wang
Keyword(s):  
Synaptic Plasticity ◽  
Nmda Receptors ◽  
Postsynaptic Density ◽  
Super Resolution ◽  
Time Lapse ◽  
Long Term Potentiation ◽  
Live Imaging ◽  
Term Potentiation ◽  
Specific Regulation

AbstractNMDA receptors (NMDAR) are key players in the initiation of synaptic plasticity that underlies learning and memory. Long-term potentiation (LTP) of synapses require an increased calcium current via NMDA channels to trigger modifications in postsynaptic density (PSD). It is generally believed that the amount of NMDARs on the postsynaptic surface remains stationary, whereas their subunit composition is dynamically fluctuated during this plasticity process. However, the molecular machinery underlying this subunit-specific regulation remains largely elusive. Here, by detecting the time-lapse changes of surface GluN2A and GluN2B subunit levels using biochemical approaches, surface immunostaining, live-imaging and super-resolution microscopy, we uncovered a transient increase of surface GluN2A-type NMDARs shortly after the induction of chemical long term potentiation (cLTP). These augmented sub-diffraction-limited GluN2A clusters predominantly exist in extrasynaptic domains. We also showed that the spine-enriched SNARE associated protein SNAP-23, and to a minor extent its homologue SNAP-25, control both the basal and regulated surface level of GluN2A receptors. Using a total internal reflection fluorescence microscopy (TIRFM) based live-imaging assay, we resolved and analyzed individual exocytic events of NMDARs in live neurons and found that cLTP raised the frequency of NMDAR exocytosis at extrasynaptic regions, without altering the duration or the package size of these events. Our study thereby provides direct evidence that synaptic plasticity controls the postsynaptic exocytosis machinery, which induces the insertion of more GluN2A receptors into the extrasynaptic area.Significance StatementMemory formation involves the long-term modification of synapses, which is called synaptic plasticity. In the postsynaptic density (PSD) of excited neurons, this modification process occurs on a minute timescale, initiated by the opening of NMDARs that trigger downstream cascades to fix the potentiation (LTP) at specific synapses for longer timescales. Here, using a novel live-imaging assay we resolved the dynamic delivery of NMDARs to the cell surface, and found that only the insertion frequency, not the duration of individual insertion or number of GluN2A subunits each of these NMDAR vesicles contains, was altered during the synaptic potentiation process. We also identified SNAP-23 as the key molecule mediating this activity dependent NMDAR surface delivery. This study provides a novel mechanism of how NMDARs are regulated in the short window to initiate the long-lasting synaptic modifications.

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