Postsynaptic Receptor Elimination During Synaptic Competition
1
Citation
13
Reference
10
Related Paper
Keywords:
Synaptic pharmacology
Synapses, points of contact between axons and dendrites, are conduits for the flow of information in the circuitry of the central nervous system. The strength of synaptic transmission reflects the interconnectedness of the axons and dendrites at synapses; synaptic strength in turn is modified by the frequency with which the synapses are stimulated. This modulation of synaptic strength, or synaptic plasticity, probably forms the cellular basis for learning and memory. RNA metabolism, particularly translational control at or near the synapse, is one process that controls long-lasting synaptic plasticity and, by extension, memory formation and consolidation. In the present paper, I review some salient features of translational control of synaptic plasticity.
Synaptic scaling
Nonsynaptic plasticity
Homosynaptic plasticity
Neuronal memory allocation
Synaptic pharmacology
Cite
Citations (22)
Traditionally, brain function is considered to be exclusive to neuronal activity. Recent studies have shown that in addition to the classical bidirectional information flow between presynaptic and postsynaptic neurons, astrocytes also participate in the process of information exchange between synaptic neurons, response to synaptic activity, and regulation of synaptic transmission. We review herein astrocytes integrate and process synaptic information and finally regulate synaptic transmission and plasticity through releasing gliotransmitters.
Key words:
Tripartite synapse; Astrocyte; Synaptic transmission; Synaptic plasticity
Synaptic scaling
Nonsynaptic plasticity
Synaptic pharmacology
Neuronal memory allocation
Cite
Citations (0)
Synaptic plasticity is vital for learning and memory in the brain. It consists of long-term potentiation (LTP) and long-term depression (LTD). Spike frequency is one of the major components of synaptic plasticity in the brain, a noisy environment. Recently, we mathematically analysed the frequency-dependent synaptic plasticity (FDP) in vivo and found that LTP is more likely to occur with an increase in the frequency of background synaptic activity. Previous studies suggest fluctuation in the amplitude of background synaptic activity. However, little is understood about the relationship between synaptic plasticity and the fluctuation in the background synaptic activity. To address this issue, we performed numerical simulations of a calcium-based synapse model. Then, we found attenuation of the tendency to become LTD due to an increase in the fluctuation of background synaptic activity, leading to an enhancement of synaptic weight. Our result suggests that the fluctuation affect synaptic plasticity in the brain.
Synaptic scaling
Nonsynaptic plasticity
Homosynaptic plasticity
Neural facilitation
Homeostatic plasticity
Cite
Citations (0)
Synaptic plasticity is vital for learning and memory in the brain. It consists of long-term potentiation (LTP) and long-term depression (LTD). Spike frequency is one of the major components of synaptic plasticity in the brain, a noisy environment. Recently, we mathematically analyzed the frequency-dependent synaptic plasticity (FDP) in vivo and found that LTP is more likely to occur with an increase in the frequency of background synaptic activity. Meanwhile, previous studies suggest statistical fluctuation in the amplitude of background synaptic activity. Little is understood, however, about its contribution to synaptic plasticity. To address this issue, we performed numerical simulations of a calcium-based synapse model. Then, we found attenuation of the tendency to become LTD due to an increase in the fluctuation of background synaptic activity, leading to an enhancement of synaptic weight. Our result suggests that the fluctuation affects synaptic plasticity in the brain.
Synaptic scaling
Nonsynaptic plasticity
Homosynaptic plasticity
Neural facilitation
Homeostatic plasticity
Cite
Citations (0)
Complex sets of nervous system functions are dependent on proper working of the synaptic apparatus, and these functions are regulated by diverse synaptic proteins that are distributed in various subcellular compartments of the synapse. The most extensively studied synaptic proteins are synaptophysin, the synapsins, growth associated protein 43 (GAP-43), SV-2, and p65. Moreover, synaptic terminals contain a great number of other proteins involved in calcium transport, neurotransmission, signaling, growth and plasticity. Probes against various synaptic proteins have recently been used to study synaptic alterations in human disease, as well as in experimental models of neurological disorders. Such probes are useful markers of synaptic function and synaptic population density in the nervous system. For the present, we will review the role of synaptic proteins in the following conditions: Alzheimer's disease (AD) and other disorders including ischemia, disorders where synapse-associated proteins are abnormally accumulated in the nerve terminals, synaptic proteins altered after denervation, and synaptic proteins as markers in neoplastic disorders. The study of the molecular alterations of the synapses and of plasticity might yield important clues as to the mechanisms of neurodegeneration in AD, and of the patterns of presynaptic and dendritic damage under diverse pathological conditions.
Synaptophysin
Synaptic pharmacology
Synaptic scaling
Nonsynaptic plasticity
Cite
Citations (141)
Synaptic plasticity is vital for learning and memory in the brain. It consists of long-term potentiation (LTP) and long-term depression (LTD). Spike frequency is one of the major components of synaptic plasticity in the brain, a noisy environment. Recently, we mathematically analysed the frequency-dependent synaptic plasticity (FDP) in vivo and found that LTP is more likely to occur with an increase in the frequency of background synaptic activity. Previous studies suggest fluctuation in the amplitude of background synaptic activity. However, little is understood about the relationship between synaptic plasticity and the fluctuation in the background synaptic activity. To address this issue, we performed numerical simulations of a calcium-based synapse model. Then, we found attenuation of the tendency to become LTD due to an increase in the fluctuation of background synaptic activity, leading to an enhancement of synaptic weight. Our result suggests that the fluctuation affect synaptic plasticity in the brain.
Synaptic scaling
Nonsynaptic plasticity
Homosynaptic plasticity
Neural facilitation
Homeostatic plasticity
Cite
Citations (0)
Abstract Bidirectional trans ‐synaptic signaling is essential for the formation, maturation, and plasticity of synaptic connections. Synaptic cell adhesion molecules (CAMs) are prime drivers in shaping the identities of trans ‐synaptic signaling pathways. A series of recent studies provide evidence that diverse presynaptic cell adhesion proteins dictate the regulation of specific synaptic properties in postsynaptic neurons. Focusing on mammalian synaptic CAMs, this article outlines several exemplary cases supporting this notion and highlights how these trans ‐synaptic signaling pathways collectively contribute to the specificity and diversity of neural circuit architecture.
Nonsynaptic plasticity
Synaptic scaling
Synaptic pharmacology
Synaptic cleft
Cite
Citations (7)
Synaptic pharmacology
Synaptic scaling
Synaptic cleft
Cite
Citations (1,643)
Background and purpose: Glial cells seem to play role in synaptic plasticity because they have the ability to release trophic factors and gliotransmitters and respond to neurotransmitters. They also play important role in synaptic space homeostasis. In this study, the role of hippocampal glial cells in baseline synaptic response and short term synaptic plasticity were investigated. Materials and methods: In this experimental study, flourocitrate, glia inhibitor (1nmol/0.5μl), was microinjected intrahippcampally for inhibition of hippocampal glial cells. Baseline synaptic response and short term synaptic plasticity were evaluated by field potential recording. fEPSP was recorded from CA1 following Schaffer collaterals stimulation. After Input/Output curve construction, short term synaptic plasticity was induced by paired pulse stimulations. Results: Inhibition of glial cells by flourocitrate microinjection in CA1 did not have any effect on baseline synaptic response (P>0.05). Flourocitrate increased paired pulse index (PPI, control: 62.80%±5.48; flourocitrate treated: 87.19%±12.11) at 20 ms inter pulse interval (P 0.05). Conclusion: The results suggest that hippocampal glial cells functions did not influence the baseline synaptic response but affected short term synaptic plasticity in CA1 area of the hippocampus.
Neural facilitation
Synaptic scaling
Nonsynaptic plasticity
Homeostatic plasticity
Cite
Citations (0)