scholarly journals Punctuated evolution of visual cortical circuits? Evidence from the large rodent Dasyprocta leporina, and the tiny primate Microcebus murinus

2021 ◽  
Vol 71 ◽  
pp. 110-118
Author(s):  
Kerstin E. Schmidt ◽  
Fred Wolf
2008 ◽  
Vol 9 (2) ◽  
pp. 97-107 ◽  
Author(s):  
Paul Tiesinga ◽  
Jean-Marc Fellous ◽  
Terrence J. Sejnowski

2021 ◽  
Vol 22 (17) ◽  
pp. 9412
Author(s):  
Gianluca Pietra ◽  
Tiziana Bonifacino ◽  
Davide Talamonti ◽  
Giambattista Bonanno ◽  
Alessandro Sale ◽  
...  

Retinitis pigmentosa (RP) is a family of inherited disorders caused by the progressive degeneration of retinal photoreceptors. There is no cure for RP, but recent research advances have provided promising results from many clinical trials. All these therapeutic strategies are focused on preserving existing photoreceptors or substituting light-responsive elements. Vision recovery, however, strongly relies on the anatomical and functional integrity of the visual system beyond photoreceptors. Although the retinal structure and optic pathway are substantially preserved at least in early stages of RP, studies describing the visual cortex status are missing. Using a well-established mouse model of RP, we analyzed the response of visual cortical circuits to the progressive degeneration of photoreceptors. We demonstrated that the visual cortex goes through a transient and previously undescribed alteration in the local excitation/inhibition balance, with a net shift towards increased intracortical inhibition leading to improved filtering and decoding of corrupted visual inputs. These results suggest a compensatory action of the visual cortex that increases the range of residual visual sensitivity in RP.


2004 ◽  
Vol 17 (5-6) ◽  
pp. 707-718 ◽  
Author(s):  
Arash Yazdanbakhsh ◽  
Stephen Grossberg

2017 ◽  
Author(s):  
Jianguang Ni (倪剑光) ◽  
Christopher Murphy Lewis ◽  
Thomas Wunderle ◽  
Patrick Jendritza ◽  
Ilka Diester ◽  
...  

AbstractActivated visual cortex typically engages in neuronal synchronization in the gamma-frequency band (30-90 Hz). Gamma-band synchronization is related to cognitive functioning, and its mechanisms have been extensively investigated, predominantly through in-vitro studies. To further elucidate its mechanisms in-vivo, we performed simultaneous optogenetic stimulation and electrophysiological recordings of visual cortical areas 17 and 21a in the anesthetized cat. Viral transfection with AAV1 or AAV9 under a CamKIIα promoter led to robust Channelrhodopsin-2 (ChR2) expression. Immunohistochemical analysis showed that all ChR2-expressing neurons were negative for Parvalbumin, consistent with predominant or exclusive expression in excitatory neurons. Optogenetic stimulation used primarily surface illumination directly above the transfected and recorded cells. Stimulation with constant light led to strong and sustained gamma-band synchronization with strength and bandwidth similar to visually induced gamma. Rhythmic stimulation with light-pulse trains or sinusoidal light modulation revealed strongest resonance for gamma-band frequencies. Gamma resonance was confirmed by optogenetic white-noise stimulation. White-noise stimulation allowed the quantification of the transfer function between the optogenetic stimulation and the local field potential response. This transfer function showed a dominant peak in the gamma band. Thus, we find that visual cortical circuits resonate most strongly to gamma-band components in their input. This resonance renders both the sensitivity to input, and the output of these circuits, selectively tuned to gamma.Significance StatementActivated groups of cortical neurons often display rhythmic synchronization in the gamma-frequency band (30-90 Hz). Gamma-band synchronization is particularly well studied in visual cortex. We used optogenetics to control visual cortex neurons with light. Different optogenetic stimulation protocols, using constant light, rhythmically modulated light or white-noise modulated light, all demonstrated that the investigated circuits predominantly resonate to stimulation in the gamma band. The observed gamma-band resonance renders visual cortical circuits most sensitive to gamma-rhythmic synaptic inputs. This in turn renders their spike output and the ensuing interareal synchronization gamma rhythmic.This work was supported by DFG (SPP 1665, FOR 1847, FR2557/5-1-CORNET to P.F.; EXC 1086, DI 1908/5-1, DI 1908/6-1 to I.D.), BMBF (01GQ1301 to I.D.), EU (HEALTH-F2-2008-200728-BrainSynch, FP7-604102-HBP, FP7-600730-Magnetrodes to P.F.; ERC Starting Grant OptoMotorPath to I.D.), a European Young Investigator Award to P.F., the FENS-Kavli Network of Excellence to I.D., National Institutes of Health (1U54MH091657-WU-Minn-Consortium-HCP to P.F.), the LOEWE program (NeFF to P.F. and I.D.). Present address of I.D.: Optophysiology, Bernstein Center and BrainLinks-BrainTools, University of Freiburg, Albertstrase 23, 79104 Freiburg, Germany.Author contributionsJ.N, C.M.L., T.W., P.F. designed research; J.N, C.M.L., T.W., P.J., I.D., P.F. performed experiments; J.N., C.M.L., T.W. analyzed data; J.N., P.F. wrote the paper.


2020 ◽  
Author(s):  
Madineh Sedigh-Sarvestani ◽  
Kuo-Sheng Lee ◽  
Rachel Satterfield ◽  
Nicole Shultz ◽  
David Fitzpatrick

The retinotopic maps of many visual cortical areas are thought to follow the fundamental principles that have been described for primary visual cortex (V1) where nearby points on the retina map to nearby points on the surface of V1, and orthogonal axes of the retinal surface are represented along orthogonal axes of the cortical surface. Here we demonstrate a striking departure from this conventional mapping in the secondary visual area (V2) of the tree shrew. Although local retinotopy is preserved, orthogonal axes of the retina are represented along the same axis of the cortical surface, an unexpected geometry explained by an orderly sinusoidal transform of the retinal surface. This sinusoidal topography is ideally suited for achieving uniform coverage in an elongated area like V2, is predicted by mathematical models designed to achieve wiring minimization, and provides a novel explanation for stripe-like patterns of intra-cortical connections and stimulus response properties in V2. Our findings suggest that cortical circuits flexibly implement solutions to sensory surface representation, with dramatic consequences for the large-scale layout of topographic maps.


2018 ◽  
Author(s):  
Vedakumar Tatavarty ◽  
Alejandro Torrado Pacheco ◽  
Heather Lin ◽  
Nathaniel J. Miska ◽  
Keith B. Hengen ◽  
...  

SummaryMutations in Shank3 are strongly associated with autism spectrum disorders and circuit disfunction, but a unified view of how Shank3 loss disrupts circuit function and excitability is lacking. Stabilizing, homeostatic forms of synaptic and intrinsic plasticity are critical for preventing circuit hyper- or hypo-excitability, leading us to ask whether Shank3 loss perturbs circuits by disrupting homeostatic plasticity. We show that Shank3 loss abolishes synaptic and intrinsic homeostatic plasticity, which can be rescued by lithium(Li), a drug with therapeutic potential in human Shankopathies. Further, Shank3 loss in vivo severely compromises the ability of visual cortical circuits to recover from perturbations to sensory drive. Our findings suggest that the loss of homeostatic compensation is a critical endophenotype that can explain a range of circuit disfunctions in Shankopathies.


Author(s):  
Guy Bouvier ◽  
Yuta Senzai ◽  
Massimo Scanziani

AbstractThe vestibular system broadcasts head-movement related signals to sensory areas throughout the brain, including visual cortex. These signals are crucial for the brain’s ability to assess whether motion of the visual scene results from the animal’s head-movements. How head-movements impact visual cortical circuits remains, however, poorly understood. Here, we discover that ambient luminance profoundly transforms how mouse primary visual cortex (V1) processes head-movements. While in darkness, head movements result in an overall suppression of neuronal activity, in ambient light the same head movements trigger excitation across all cortical layers. This light-dependent switch in how V1 processes head-movements is controlled by somatostatin expressing (SOM) inhibitory neurons, which are excited by head movements in dark but not in light. This study thus reveals a light-dependent switch in the response of V1 to head-movements and identifies a circuit in which SOM cells are key integrators of vestibular and luminance signals.


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