scholarly journals Loss of Sensory Input Causes Rapid Structural Changes of Inhibitory Neurons in Adult Mouse Visual Cortex

Neuron ◽  
2011 ◽  
Vol 71 (5) ◽  
pp. 869-882 ◽  
Author(s):  
Tara Keck ◽  
Volker Scheuss ◽  
R. Irene Jacobsen ◽  
Corette J. Wierenga ◽  
Ulf T. Eysel ◽  
...  
2016 ◽  
Vol 115 (4) ◽  
pp. 1821-1835 ◽  
Author(s):  
Cristin G. Welle ◽  
Diego Contreras

Gamma oscillations are a robust component of sensory responses but are also part of the background spontaneous activity of the brain. To determine whether the properties of gamma oscillations in cortex are specific to their mechanism of generation, we compared in mouse visual cortex in vivo the laminar geometry and single-neuron rhythmicity of oscillations produced during sensory representation with those occurring spontaneously in the absence of stimulation. In mouse visual cortex under anesthesia (isoflurane and xylazine), visual stimulation triggered oscillations mainly between 20 and 50 Hz, which, because of their similar functional significance to gamma oscillations in higher mammals, we define here as gamma range. Sensory representation in visual cortex specifically increased gamma oscillation amplitude in the supragranular (L2/3) and granular (L4) layers and strongly entrained putative excitatory and inhibitory neurons in infragranular layers, while spontaneous gamma oscillations were distributed evenly through the cortical depth and primarily entrained putative inhibitory neurons in the infragranular (L5/6) cortical layers. The difference in laminar distribution of gamma oscillations during the two different conditions may result from differences in the source of excitatory input to the cortex. In addition, modulation of superficial gamma oscillation amplitude did not result in a corresponding change in deep-layer oscillations, suggesting that superficial and deep layers of cortex may utilize independent but related networks for gamma generation. These results demonstrate that stimulus-driven gamma oscillations engage cortical circuitry in a manner distinct from spontaneous oscillations and suggest multiple networks for the generation of gamma oscillations in cortex.


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.


2019 ◽  
Vol 10 (1) ◽  
Author(s):  
Thomas Knöpfel ◽  
Yann Sweeney ◽  
Carola I. Radulescu ◽  
Nawal Zabouri ◽  
Nazanin Doostdar ◽  
...  

AbstractWe experience the world through multiple senses simultaneously. To better understand mechanisms of multisensory processing we ask whether inputs from two senses (auditory and visual) can interact and drive plasticity in neural-circuits of the primary visual cortex (V1). Using genetically-encoded voltage and calcium indicators, we find coincident audio-visual experience modifies both the supra and subthreshold response properties of neurons in L2/3 of mouse V1. Specifically, we find that after audio-visual pairing, a subset of multimodal neurons develops enhanced auditory responses to the paired auditory stimulus. This cross-modal plasticity persists over days and is reflected in the strengthening of small functional networks of L2/3 neurons. We find V1 processes coincident auditory and visual events by strengthening functional associations between feature specific assemblies of multimodal neurons during bouts of sensory driven co-activity, leaving a trace of multisensory experience in the cortical network.


2015 ◽  
Vol 5 (1) ◽  
Author(s):  
L. Ruiz-Perera ◽  
M. Muniz ◽  
G. Vierci ◽  
N. Bornia ◽  
L. Baroncelli ◽  
...  

2017 ◽  
Author(s):  
Kyle R. Jenks ◽  
Taekeun Kim ◽  
Elissa D. Pastuzyn ◽  
Hiroyuki Okuno ◽  
Andrew V. Taibi ◽  
...  

AbstractThe molecular basis for the decline in experience-dependent neural plasticity over age remains poorly understood. In visual cortex, the robust plasticity induced in juvenile mice by brief monocular deprivation (MD) during the critical period is abrogated by genetic deletion of Arc, an activity-dependent regulator of excitatory synaptic modification. Here we report that augmenting Arc expression in adult mice prolongs juvenile-like plasticity in visual cortex, as assessed by recordings of ocular dominance (OD) plasticity in vivo. A distinguishing characteristic of juvenile OD plasticity is the weakening of deprived-eye responses, believed to be accounted for by the mechanisms of homosynaptic long-term depression (LTD). Accordingly, we also found increased LTD in visual cortex of adult mice with augmented Arc expression, and impaired LTD in visual cortex of juvenile mice that lack Arc or have been treated in vivo with a protein synthesis inhibitor. Further, we found that although activity-dependent expression of Arc mRNA does not change with age, expression of Arc protein is maximal during the critical period and declines in adulthood. Finally, we show that acute augmentation of Arc expression in wild type adult mouse visual cortex is sufficient to restore juvenile-like plasticity. Together, our findings suggest a unifying molecular explanation for the age- and activity-dependent modulation of synaptic sensitivity to deprivation.Significance StatementNeuronal plasticity peaks early in life during critical periods and normally declines with age, but the molecular changes that underlie this decline are not fully understood. Using the mouse visual cortex as a model, we found that activity-dependent expression of the neuronal protein Arc peaks early in life, and that loss of activity-dependent Arc expression parallels loss of synaptic plasticity in the visual cortex. Genetic overexpression of Arc prolongs the critical period of visual cortex plasticity and acute viral expression of Arc in adult mice can restore juvenile-like plasticity. These findings provide a mechanism for the loss of excitatory plasticity with age, and suggest that Arc may be an exciting therapeutic target for modulation of the malleability of neuronal circuits.


2020 ◽  
Vol 40 (27) ◽  
pp. 5214-5227 ◽  
Author(s):  
Masato Sadahiro ◽  
Michael P. Demars ◽  
Poromendro Burman ◽  
Priscilla Yevoo ◽  
Andreas Zimmer ◽  
...  

2014 ◽  
Vol 25 (10) ◽  
pp. 3713-3722 ◽  
Author(s):  
M. Hadi Saiepour ◽  
Sridhara Chakravarthy ◽  
Rogier Min ◽  
Christiaan N. Levelt

2003 ◽  
Vol 464 (4) ◽  
pp. 426-437 ◽  
Author(s):  
Akiko Yamashita ◽  
Katia Valkova ◽  
Yuri Gonchar ◽  
Andreas Burkhalter

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