scholarly journals Stability and plasticity of contextual modulation in the mouse visual cortex

2016 ◽  
Author(s):  
Adam Ranson

SummaryActivity of neurons in primary sensory cortex is shaped by visual and behavioural context. However the long-term stability of the influence of contextual factors in the mature cortex remains poorly understood. To investigate this we used 2-photon calcium imaging to track the influence of surround suppression and locomotion on individual neurons over 14 days. We found that highly active excitatory neurons and PV+ interneurons exhibited relatively stable modulation by visual context. Similarly most neurons exhibited a stable yet distinct degree modulation by locomotion. In contrast less active excitatory neurons exhibited plasticity in visual context influence resulting in increased suppression. These findings suggest that the mature visual cortex possesses stable subnetworks of neurons, differentiated by cell-type and activity level, which have distinctive and stable interactions with sensory and behavioural context, as well as other less active and more labile neurons which are sensitive to visual experience.

Author(s):  
Andreas J. Keller ◽  
Mario Dipoppa ◽  
Morgane M. Roth ◽  
Matthew S. Caudill ◽  
Alessandro Ingrosso ◽  
...  

Context guides perception by influencing the saliency of sensory stimuli. Accordingly, in visual cortex, responses to a stimulus are modulated by context, the visual scene surrounding the stimulus. Responses are suppressed when stimulus and surround are similar but not when they differ. The mechanisms that remove suppression when stimulus and surround differ remain unclear. Here we use optical recordings, manipulations, and computational modelling to show that a disinhibitory circuit consisting of vasoactive-intestinal-peptide-expressing (VIP) and somatostatin-expressing (SOM) inhibitory neurons modulates responses in mouse visual cortex depending on the similarity between stimulus and surround. When the stimulus and the surround are similar, VIP neurons are inactive and SOM neurons suppress excitatory neurons. However, when the stimulus and the surround differ, VIP neurons are active, thereby inhibiting SOM neurons and relieving excitatory neurons from suppression. We have identified a canonical cortical disinhibitory circuit which contributes to contextual modulation and may regulate perceptual saliency.


2020 ◽  
Author(s):  
Shumsuzzaman Khan

AbstractIn reward-based learning, synaptic eligibility traces are a well-defined theoretical solution for the conversion of initial co-activation of pre and postsynaptic neurons into long-term changes in synaptic strength by reward-linked neuromodulators. However, the types of neuromodulators involved in such a phenomenon in mouse visual cortex remain unknown. To characterize the Ex vivo condition, we used optogenetic stimulation of channelrhodopsin-(ChR2) expressing Cre/Ai32(ChR2-eYFP); Tph2-Cre/Ai32(ChR2-eYFP); Thi-Cre/Ai32(ChR2-eYFP) homozygous mice, which release acetylcholine, serotonin, and norepinephrine, respectively. With these mice it is possible to measure the transformation of eligibility traces into long-term changes by endogenous neuromodulators. Here we delineated that layer 2/3 neurons in the visual cortex showed no LTD after conditioning with paired-pulse low-frequency stimulation (ppLFS; 2Hz, 15 min). However, if conditioning was paired with acetylcholine, serotonin, or norepinephrine release upon 473 nm optical stimulation in brain slices, LTD occurs in every case. Thus, our data suggests a new pathway to connect the gap between stimulus and reward. Moreover, we found that stimulation by theta-glass or metal stimulators evoked IPSC traces with the same amplitudes but differences in decay kinetics, further questioning the appropriate use of stimulators in brain slices for evoking an event.


Author(s):  
Teresa Sierpińska

Tooth wear is considered a normal, age dependent, physiological process that leads to the loss of enamel and dentine. However, in some cases the process is so progressive that it may be pathologic. The focus of this chapter is to present the consequences of advanced tooth wear resultant from parafunction, excessive masticatory forces, imbalanced occlusal contacts, and hyperactive masticatory muscles. This chapter also outlines preventative strategies that can predictably reduce the progression of pathologic wear, which employ the T-Scan 8/BioEMG synchronization module. These two objective companion technologies assess the occlusion before, during, and after dental treatment, as well as predictably control the long-term stability of newly installed fixed, implant-supported, or removable prostheses. Their synchronization correlates muscle activity level information directly to occlusal contact force and time-sequencing information, which when applied together in the wear patient can be instrumental in tempering and eliminating pathologic occlusal wear.


2018 ◽  
Vol 223 (5) ◽  
pp. 2073-2095 ◽  
Author(s):  
Isabelle Scheyltjens ◽  
Samme Vreysen ◽  
Chris Van den Haute ◽  
Victor Sabanov ◽  
Detlef Balschun ◽  
...  

2013 ◽  
Vol 33 (18) ◽  
pp. 7787-7798 ◽  
Author(s):  
M. K. Arami ◽  
K. Sohya ◽  
A. Sarihi ◽  
B. Jiang ◽  
Y. Yanagawa ◽  
...  

Cell Reports ◽  
2014 ◽  
Vol 9 (5) ◽  
pp. 1896-1907 ◽  
Author(s):  
Teppei Ebina ◽  
Kazuhiro Sohya ◽  
Itaru Imayoshi ◽  
Shu-Ting Yin ◽  
Rui Kimura ◽  
...  

2021 ◽  
Author(s):  
Shumsuzzaman Khan

Abstract In reward-based learning, synaptic eligibility traces are a well-defined theoretical solution for the conversion of initial co-activation of pre and postsynaptic neurons into long-term changes in synaptic strength by reward-linked neuromodulators. However, the types of neuromodulators involved in such a phenomenon in mouse visual cortex remain unknown. To characterize the Ex vivo condition, we used optogenetic stimulation of channelrhodopsin-(ChR2) expressing Cre/Ai32(ChR2-eYFP); Tph2-Cre/Ai32(ChR2-eYFP); Thi-Cre/Ai32(ChR2-eYFP) homozygous mice, which release acetylcholine, serotonin, and norepinephrine, respectively. With these mice it is possible to measure the transformation of eligibility traces into long-term changes by endogenous neuromodulators. Here we delineated that layer 2/3 neurons in the visual cortex showed no LTD after conditioning with paired-pulse low-frequency stimulation (ppLFS; 2Hz, 15 min). However, if conditioning was paired with acetylcholine, serotonin, or norepinephrine release upon 473 nm optical stimulation in brain slices, LTD occurs in every case. Thus, our data suggests a new pathway to connect the gap between stimulus and reward. Moreover, we found that stimulation by theta-glass or metal stimulators evoked IPSC traces with the same amplitudes but differences in decay kinetics, further questioning the appropriate use of stimulators in brain slices for evoking an event.


2017 ◽  
Author(s):  
Wuqiang Guan ◽  
Jun-Wei Cao ◽  
Lin-Yun Liu ◽  
Zhi-Hao Zhao ◽  
Yinghui Fu ◽  
...  

AbstractEye opening, a natural and timed event during animal development, influences cortical circuit assembly and maturation; yet, little is known about its precise effect on inhibitory synaptic connections. Here we show that coinciding with eye opening, the strength of unitary inhibitory postsynaptic currents (uIPSCs) from somatostatin-expressing interneurons (SST-INs) to nearby excitatory neurons, but not interneurons, sharply decreases in layer 2/3 of the mouse visual cortex. In contrast, the strength of uIPSCs from fast-spiking interneurons (FS-INs) to excitatory neurons significantly increases during eye opening. More importantly, these developmental changes can be prevented by dark rearing or binocular lid suture, and reproduced by artificial opening of sutured lids. Mechanistically, this differential maturation of synaptic transmission is accompanied by a significant change in the postsynaptic quantal size. Together, our study reveals a differential regulation in GABAergic circuits in the cortex driven by eye opening likely crucial for cortical maturation and function.


2000 ◽  
Author(s):  
Jack L. Lewis

Abstract Tissue engineering of cartilage and other connective tissues is a highly active area of research, motivated by the considerable medical need and commercial potential. Tissue with biological properties and biochemical composition similar to cartilage have been generated in laboratory cultures and animal models, and one method is being used in patients. Throughout the early development of regenerated cartilage, the focus has been on getting something to grow that is biochemically like cartilage and fills defects with tissue that visually looks like cartilage and holds up mechanically over the short term. The issues of cell source, culturing conditions, and scaffolds have also been addressed. However, all of the tissues generated have structure and microstructural organization that are not like natural cartilage. Although the clinical performance of the regenerated tissue appears promising, experience with prior regenerated tissue and the fact that the tissue is abnormal gives concern about the long term performance of the regenerated cartilage and the influence of activity level on this performance. Its long term mechanical properties are suspected to be inadequate. Future developments in this area will need to both enhance the mechanical characteristics of the regenerated tissue and develop methods and criteria for evaluating the tissue that is generated. Our work on matrix assembly by chondrocytes has been directed towards these ends. The goal has been to understand the microstructural basis for mechanical properties in tissue generated by chondrocytes in culture, develop methods to alter and control the microstructure, and build both experimental and theoretical models that allow evaluating the connection between microstructure and macroscopic properties. This is similar to a materials science approach which, we believe, will be one approach to the second generation of engineered tissues. The approach and results to date on tissue generated by chondrocytes will be described in this presentation. A specific question related to collagen network microstructure will be used to illustrate this approach.


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