scholarly journals Disruption of NMDAR Function Prevents Normal Experience-Dependent Homeostatic Synaptic Plasticity in Mouse Primary Visual Cortex

2019 ◽  
Vol 39 (39) ◽  
pp. 7664-7673 ◽  
Author(s):  
Gabriela Rodriguez ◽  
Lukas Mesik ◽  
Ming Gao ◽  
Samuel Parkins ◽  
Rinki Saha ◽  
...  
Keyword(s):  
Synaptic Plasticity ◽  
Visual Cortex ◽  
Primary Visual Cortex ◽  
Homeostatic Synaptic Plasticity

scholarly journals BACE1 Is Necessary for Experience-Dependent Homeostatic Synaptic Plasticity in Visual Cortex

2014 ◽  
Vol 2014 ◽  
pp. 1-7 ◽  
Author(s):  
Emily Petrus ◽  
Hey-Kyoung Lee
Keyword(s):  
Synaptic Plasticity ◽  
Visual Cortex ◽  
Synaptic Transmission ◽  
Sensory Experience ◽  
Synaptic Function ◽  
Excitatory Synaptic Transmission ◽  
Early Gene ◽  
Dependent Manner ◽  
Homeostatic Synaptic Plasticity ◽  
Activity Dependent

Alzheimer’s disease (AD) is the most common form of age-related dementia, which is thought to result from overproduction and/or reduced clearance of amyloid-beta (Aβ) peptides. Studies over the past few decades suggest that Aβis produced in an activity-dependent manner and has physiological relevance to normal brain functions. Similarly, physiological functions forβ- andγ-secretases, the two key enzymes that produce Aβby sequentially processing the amyloid precursor protein (APP), have been discovered over recent years. In particular, activity-dependent production of Aβhas been suggested to play a role in homeostatic regulation of excitatory synaptic function. There is accumulating evidence that activity-dependent immediate early gene Arc is an activity “sensor,” which acts upstream of Aβproduction and triggers AMPA receptor endocytosis to homeostatically downregulate the strength of excitatory synaptic transmission. We previously reported that Arc is critical for sensory experience-dependent homeostatic reduction of excitatory synaptic transmission in the superficial layers of visual cortex. Here we demonstrate that mice lacking the major neuronalβ-secretase, BACE1, exhibit a similar phenotype: stronger basal excitatory synaptic transmission and failure to adapt to changes in visual experience. Our results indicate that BACE1 plays an essential role in sensory experience-dependent homeostatic synaptic plasticity in the neocortex.

Age-Dependent Decline in Supragranular Long-Term Synaptic Plasticity by Increased Inhibition During the Critical Period in the Rat Primary Visual Cortex

2009 ◽  
Vol 101 (1) ◽  
pp. 269-275 ◽  
Author(s):  
Hyun-Jong Jang ◽  
Kwang-Hyun Cho ◽  
Hyun-Sok Kim ◽  
Sang June Hahn ◽  
Myung-Suk Kim ◽  
...  
Keyword(s):  
Synaptic Plasticity ◽  
Visual Cortex ◽  
Primary Visual Cortex ◽  
Critical Period ◽  
Excitatory Postsynaptic Potential ◽  
Age Dependent ◽  
Layer 4 ◽  
Old Rats ◽  
Synaptic Model

Supragranular long-term potentiation (LTP) and depression (LTD) are continuously induced in the pathway from layer 4 during the critical period in the rodent primary visual cortex, which limits the use of supragranular long-term synaptic plasticity as a synaptic model for the mechanism of ocular dominance (OD) plasticity. The results of the present study demonstrate that the pulse duration of extracellular stimulation to evoke a field potential (FP) is critical to induction of LTP and LTD in this pathway. LTP and LTD were induced in the pathway from layer 4 to layer 2/3 in slices from 3-wk-old rats when FPs were evoked by 0.1- and 0.2-ms pulses. LTP and LTD were induced in slices from 5-wk-old rats when evoked by stimulation with a 0.2-ms pulse but not by stimulation with a 0.1-ms pulse. Both the inhibitory component of FP and the inhibitory/excitatory postsynaptic potential amplitude ratio evoked by stimulation with a 0.1-ms pulse were greater than the values elicited by a 0.2-ms pulse. Stimulation with a 0.1-ms pulse at various intensities that showed the similar inhibitory FP component with the 0.2-ms pulse induced both LTD and LTP in 5-wk-old rats. Thus extracellular stimulation with shorter-duration pulses at higher intensity resulted in greater inhibition than that observed with longer-duration pulses at low intensity. This increased inhibition might be involved in the age-dependent decline of synaptic plasticity during the critical period. These results provide an alternative synaptic model for the mechanism of OD plasticity.

scholarly journals Optimal compensation for neuron death

2015 ◽  
Author(s):  
David Barrett ◽  
Sophie Deneve ◽  
Christian Machens
Keyword(s):  
Synaptic Plasticity ◽  
Visual Cortex ◽  
Primary Visual Cortex ◽  
Neural Circuits ◽  
Brain Lesions ◽  
Compensatory Mechanism ◽  
Neuron Death ◽  
Tuning Curves ◽  
Neural Damage ◽  
The Brain

The brain has an impressive ability to withstand neural damage. Diseases that kill neurons can go unnoticed for years, and incomplete brain lesions or silencing of neurons often fail to produce any effect. How does the brain compensate for such damage, and what are the limits of this compensation? We propose that neural circuits optimally compensate for neuron death, thereby preserving their function as much as possible. We show that this compensation can explain changes in tuning curves induced by neuron silencing across a variety of systems, including the primary visual cortex. We find that optimal compensation can be implemented through the dynamics of networks with a tight balance of excitation and inhibition, without requiring synaptic plasticity. The limits of this compensatory mechanism are reached when excitation and inhibition become unbalanced, thereby demarcating a recovery boundary, where signal representation fails and where diseases may become symptomatic.

scholarly journals How Sleep Shapes Thalamocortical Circuit Function in the Visual System

2019 ◽  
Vol 5 (1) ◽  
pp. 295-315 ◽  
Author(s):  
Jaclyn M. Durkin ◽  
Sara J. Aton
Keyword(s):  
Synaptic Plasticity ◽  
Visual Cortex ◽  
Primary Visual Cortex ◽  
Memory Consolidation ◽  
Cognitive Functions ◽  
Declarative Memory ◽  
Visual Response ◽  
And Function ◽  
Circuit Function

Recent data have shown that sleep plays a beneficial role for cognitive functions such as declarative memory consolidation and perceptual learning. In this article, we review recent findings on the role of sleep in promoting adaptive visual response changes in the lateral geniculate nucleus and primary visual cortex following novel visual experiences. We discuss these findings in the context of what is currently known about how sleep affects the activity and function of thalamocortical circuits and current hypotheses regarding how sleep facilitates synaptic plasticity.

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