Anatomy and electrophysiology of fast central synapses lead to a structural model for long-term potentiation

1995 ◽  
Vol 75 (4) ◽  
pp. 759-787 ◽  
Author(s):  
F. A. Edwards
Keyword(s):  
Structural Model ◽  
Long Term Potentiation ◽  
Postsynaptic Membrane ◽  
Detailed Knowledge ◽  
Excitatory Synapses ◽  
Term Potentiation ◽  
Gabaergic Synapses ◽  
Electrophysiological Findings ◽  
Central Synapses

Detailed knowledge of the anatomy of central synapses is essential to the interpretation of the vast quantity of electrophysiological findings that have been published in recent years. When their function is considered, it is not surprising that, in both anatomy and electrophysiology, fast central synapses show important differences to the neuromuscular junction. This review concentrates on the detailed anatomy of the common excitatory synapses that impinge on dendritic spines, but also refers to other glutamatergic and GABAergic synapses. This information is brought together with present knowledge of the electrophysiology of fast neurotransmission in the brain. Various types of evidence are outlined, explaining why it is now widely accepted that release of transmitter from a single vesicle virtually saturates the small number of receptors available on the postsynaptic membrane of central synapses. Finally, the anatomic literature suggests that a particular type of spine synapse, which electron microscopy reveals to have a perforated active zone, may represent a synapse with high efficacy. This suggestion is shown to be completely compatible with the electrophysiological data, and a model is presented that shows that all the apparently conflicting data in the field of long-term potentiation could be compatible. This stresses the need for cooperative collaboration between laboratories that have apparently conflicting findings.

scholarly journals Chemical LTD, but not LTP, induces transient accumulation of gelsolin in dendritic spines

2019 ◽  
Vol 400 (9) ◽  
pp. 1129-1139 ◽  
Author(s):  
Iryna Hlushchenko ◽  
Pirta Hotulainen
Keyword(s):  
Synaptic Plasticity ◽  
Dendritic Spines ◽  
Hippocampal Neurons ◽  
Long Term Potentiation ◽  
Excitatory Synapses ◽  
Signal Molecule ◽  
Brain Functions ◽  
Dendritic Shaft ◽  
Term Potentiation

Abstract Synaptic plasticity underlies central brain functions, such as learning. Ca2+ signaling is involved in both strengthening and weakening of synapses, but it is still unclear how one signal molecule can induce two opposite outcomes. By identifying molecules, which can distinguish between signaling leading to weakening or strengthening, we can improve our understanding of how synaptic plasticity is regulated. Here, we tested gelsolin’s response to the induction of chemical long-term potentiation (cLTP) or long-term depression (cLTD) in cultured rat hippocampal neurons. We show that gelsolin relocates from the dendritic shaft to dendritic spines upon cLTD induction while it did not show any relocalization upon cLTP induction. Dendritic spines are small actin-rich protrusions on dendrites, where LTD/LTP-responsive excitatory synapses are located. We propose that the LTD-induced modest – but relatively long-lasting – elevation of Ca2+ concentration increases the affinity of gelsolin to F-actin. As F-actin is enriched in dendritic spines, it is probable that increased affinity to F-actin induces the relocalization of gelsolin.

scholarly journals Inhibition promotes long-term potentiation at cerebellar excitatory synapses

2016 ◽  
Vol 6 (1) ◽  
Author(s):  
F. Binda ◽  
K. Dorgans ◽  
S. Reibel ◽  
K. Sakimura ◽  
M. Kano ◽  
...  
Keyword(s):  
Long Term Potentiation ◽  
Excitatory Synapses ◽  
Term Potentiation

Calcium: A Trigger for Long-Term Depression and Potentiation in the Hippocampus

Physiology ◽  
1994 ◽  
Vol 9 (6) ◽  
pp. 256-260
Author(s):  
D Debanne ◽  
SM Thompson
Keyword(s):  
Protein Kinases ◽  
Long Term Potentiation ◽  
Receptor Activation ◽  
Synaptic Strength ◽  
Excitatory Synapses ◽  
Long Term Depression ◽  
Aspartate Receptor ◽  
Term Potentiation ◽  
Different Levels

Two opposing types of plasticity at excitatory synapses in the hippocampus, long-term potentiation and depression, require N-methyl-D-aspartate receptor activation and Ca2+ influx for their induction.The direction of the change in synaptic strength is determined by a balance between phosphorylation and dephosphorylation, as regulated by protein kinases and phosphatases that are activated selectively by different levels of intracellular Ca2+.

scholarly journals Moderate AMPA receptor clustering on the nanoscale can efficiently potentiate synaptic current

2014 ◽  
Vol 369 (1633) ◽  
pp. 20130167 ◽  
Author(s):  
Leonid P. Savtchenko ◽  
Dmitri A. Rusakov
Keyword(s):  
Nmda Receptor ◽  
Ampa Receptors ◽  
Monte Carlo Model ◽  
Release Site ◽  
Synaptic Cleft ◽  
Long Term Potentiation ◽  
Term Potentiation ◽  
Central Synapses ◽  
Prevailing View

The prevailing view at present is that postsynaptic expression of the classical NMDA receptor-dependent long-term potentiation relies on an increase in the numbers of local AMPA receptors (AMPARs). This is thought to parallel an expansion of postsynaptic cell specializations, for instance dendritic spine heads, which accommodate synaptic receptor proteins. However, glutamate released into the synaptic cleft can normally activate only a hotspot of low-affinity AMPARs that occur in the vicinity of the release site. How the enlargement of the AMPAR pool is causally related to the potentiated AMPAR current remains therefore poorly understood. To understand possible scenarios of postsynaptic potentiation, here we explore a detailed Monte Carlo model of the typical small excitatory synapse. Simulations suggest that approximately 50% increase in the synaptic AMPAR current could be provided by expanding the existing AMPAR pool at the expense of 100–200% new AMPARs added at the same packing density. Alternatively, reducing the inter-receptor distances by only 30–35% could achieve a similar level of current potentiation without any changes in the receptor numbers. The NMDA receptor current also appears sensitive to the NMDA receptor crowding. Our observations provide a quantitative framework for understanding the ‘resource-efficient’ ways to enact use-dependent changes in the architecture of central synapses.

scholarly journals Activity-Induced Long-Term Potentiation of Excitatory Synapses in Developing Zebrafish Retina In Vivo

Neuron ◽  
2012 ◽  
Vol 75 (3) ◽  
pp. 479-489 ◽  
Author(s):  
Hong-ping Wei ◽  
Yuan-yuan Yao ◽  
Rong-wei Zhang ◽  
Xiao-feng Zhao ◽  
Jiu-lin Du
Keyword(s):  
Long Term Potentiation ◽  
Excitatory Synapses ◽  
Term Potentiation

Presynaptic Activity and Ca2+ Entry Are Required for the Maintenance of NMDA Receptor–Independent LTP at Visual Cortical Excitatory Synapses

2004 ◽  
Vol 92 (2) ◽  
pp. 1077-1087 ◽  
Author(s):  
Hong Nian Liu ◽  
Tohru Kurotani ◽  
Ming Ren ◽  
Kazumasa Yamada ◽  
Yumiko Yoshimura ◽  
...  
Keyword(s):  
Nmda Receptor ◽  
Long Term Potentiation ◽  
Inhibitory Synapses ◽  
Excitatory Synapses ◽  
Test Stimulation ◽  
Term Potentiation ◽  
Pharmacological Blockade ◽  
Visual Cortical ◽  
P Type

We have shown that some neural activity is required for the maintenance of long-term potentiation (LTP) at visual cortical inhibitory synapses. We tested whether this was also the case in N-methyl-d-aspartate (NMDA) receptor–independent LTP of excitatory connections in layer 2/3 cells of developing rat visual cortex. This LTP occurred after 2-Hz stimulation was applied for 15 min and always persisted for several hours while test stimulation was continued at 0.1 Hz. When test stimulation was stopped for 1 h after LTP induction, only one-third of the LTP instances disappeared, but most did disappear under a pharmacological suppression of spontaneous firing, indicating that LTP maintenance requires either evoked or spontaneous activities. LTP was totally abolished by a temporary blockade of action potentials with lidocaine or the removal of extracellular Ca2+ after LTP induction, but it persisted under a voltage clamp of postsynaptic cells or after a temporary blockade of postsynaptic activity with the glutamate receptor antagonist kynurenate, suggesting that LTP maintenance requires presynaptic, but not postsynaptic, firing and Ca2+ entry. More than one-half of the LTP instances were abolished after a pharmacological blockade of P-type Ca2+ channels, whereas it persisted after either L-type or Ni2+-sensitive Ca2+ channel blockades. These results show that the maintenance of NMDA receptor–independent excitatory LTP requires presynaptic firing and Ca2+ channel activation as inhibitory LTP, although the necessary level of firing and Ca2+ entry seems lower for the former than the latter and the Ca2+ channel types involved are only partly the same.

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