scholarly journals Optimal compensation for neuron death

2015 ◽  
Author(s):  
David Barrett ◽  
Sophie Deneve ◽  
Christian Machens

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.

eLife ◽  
2016 ◽  
Vol 5 ◽  
Author(s):  
David GT Barrett ◽  
Sophie Denève ◽  
Christian K Machens

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 behavioral effect. How does the brain compensate for such damage, and what are the limits of this compensation? We propose that neural circuits instantly compensate for neuron loss, 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 compensatory mechanisms 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.


2017 ◽  
Vol 372 (1715) ◽  
pp. 20160504 ◽  
Author(s):  
Megumi Kaneko ◽  
Michael P. Stryker

Mechanisms thought of as homeostatic must exist to maintain neuronal activity in the brain within the dynamic range in which neurons can signal. Several distinct mechanisms have been demonstrated experimentally. Three mechanisms that act to restore levels of activity in the primary visual cortex of mice after occlusion and restoration of vision in one eye, which give rise to the phenomenon of ocular dominance plasticity, are discussed. The existence of different mechanisms raises the issue of how these mechanisms operate together to converge on the same set points of activity. This article is part of the themed issue ‘Integrating Hebbian and homeostatic plasticity’.


Some computational theories of motion perception assume that the first stage en route to this perception is the local estimate of image velocity. However, this assumption is not supported by data from the primary visual cortex. Its motion sensitive cells are not selective to velocity, but rather are directionally selective and tuned to spatio-temporal frequen­cies. Accordingly, physiologically based theories start with filters selec­tive to oriented spatio-temporal frequencies. This paper shows that computational and physiological theories do not necessarily conflict, because such filters may, as a population, compute velocity locally. To prove this point, we show how to combine the outputs of a class of frequency tuned filters to detect local image velocity. Furthermore, we show that the combination of filters may simulate ‘Pattern’ cells in the middle temporal area (MT), whereas each filter simulates primary visual cortex cells. These simulations include three properties of the primary cortex. First, the spatio-temporal frequency tuning curves of the in­dividual filters display approximate space-time separability. Secondly, their direction-of-motion tuning curves depend on the distribution of orientations of the components of the Fourier decomposition and speed of the stimulus. Thirdly, the filters show facilitation and suppression for responses to apparent motions in the preferred and null directions, respect­ively. It is suggested that the MT’s role is not to solve the aperture problem, but to estimate velocities from primary cortex information. The spatial integration that accounts for motion coherence may be postponed to a later cortical stage.


2016 ◽  
Vol 23 (5) ◽  
pp. 529-541 ◽  
Author(s):  
Sara Ajina ◽  
Holly Bridge

Damage to the primary visual cortex removes the major input from the eyes to the brain, causing significant visual loss as patients are unable to perceive the side of the world contralateral to the damage. Some patients, however, retain the ability to detect visual information within this blind region; this is known as blindsight. By studying the visual pathways that underlie this residual vision in patients, we can uncover additional aspects of the human visual system that likely contribute to normal visual function but cannot be revealed under physiological conditions. In this review, we discuss the residual abilities and neural activity that have been described in blindsight and the implications of these findings for understanding the intact system.


Perception ◽  
10.1068/p5338 ◽  
2005 ◽  
Vol 34 (11) ◽  
pp. 1339-1352 ◽  
Author(s):  
Ernest Greene ◽  
William Frawley

In previous studies, we have found that the accuracy in judging collinearity of lines or dots varies considerably from one subject to another as a function of the relative angle of the stimulus elements. A model of errors generally shows large excursions across several subranges of angular position. These do not appear to be motor errors, at least not ones that are well separated from perceptual mechanisms. The errors are most likely generated at primary visual cortex, or beyond. We examined and modeled accuracy in judging collinearity of dot pairs, varying the angular position of the dots through 360°, the distance between the dots (stimulus span), and the distance at which the subject was required to respond (response span). Subjects manifested idiosyncratic profiles of error across angular positions, as reported previously. But across the tested range of spans, from 4 to 8 deg, the errors tended to be the same, irrespective of stimulus or response span. This suggests that the judgments are based on a radial (angular) measure of spatial position. We discuss these results in the context of proposals that the brain maps spatial position using rotation coordinates. These new data are consistent with the hypothesis that subjects use the z-axis coordinates as a mental protractor for judging angular position and collinearity.


2013 ◽  
Vol 110 (4) ◽  
pp. 964-972 ◽  
Author(s):  
Agne Vaiceliunaite ◽  
Sinem Erisken ◽  
Florian Franzen ◽  
Steffen Katzner ◽  
Laura Busse

Responses of many neurons in primary visual cortex (V1) are suppressed by stimuli exceeding the classical receptive field (RF), an important property that might underlie the computation of visual saliency. Traditionally, it has proven difficult to disentangle the underlying neural circuits, including feedforward, horizontal intracortical, and feedback connectivity. Since circuit-level analysis is particularly feasible in the mouse, we asked whether neural signatures of spatial integration in mouse V1 are similar to those of higher-order mammals and investigated the role of parvalbumin-expressing (PV+) inhibitory interneurons. Analogous to what is known from primates and carnivores, we demonstrate that, in awake mice, surround suppression is present in the majority of V1 neurons and is strongest in superficial cortical layers. Anesthesia with isoflurane-urethane, however, profoundly affects spatial integration: it reduces the laminar dependency, decreases overall suppression strength, and alters the temporal dynamics of responses. We show that these effects of brain state can be parsimoniously explained by assuming that anesthesia affects contrast normalization. Hence, the full impact of suppressive influences in mouse V1 cannot be studied under anesthesia with isoflurane-urethane. To assess the neural circuits of spatial integration, we targeted PV+ interneurons using optogenetics. Optogenetic depolarization of PV+ interneurons was associated with increased RF size and decreased suppression in the recorded population, similar to effects of lowering stimulus contrast, suggesting that PV+ interneurons contribute to spatial integration by affecting overall stimulus drive. We conclude that the mouse is a promising model for circuit-level mechanisms of spatial integration, which relies on the combined activity of different types of inhibitory interneurons.


2003 ◽  
Vol 20 (1) ◽  
pp. 77-84 ◽  
Author(s):  
AN CAO ◽  
PETER H. SCHILLER

Relative motion information, especially relative speed between different input patterns, is required for solving many complex tasks of the visual system, such as depth perception by motion parallax and motion-induced figure/ground segmentation. However, little is known about the neural substrate for processing relative speed information. To explore the neural mechanisms for relative speed, we recorded single-unit responses to relative motion in the primary visual cortex (area V1) of rhesus monkeys while presenting sets of random-dot arrays moving at different speeds. We found that most V1 neurons were sensitive to the existence of a discontinuity in speed, that is, they showed higher responses when relative motion was presented compared to homogenous field motion. Seventy percent of the neurons in our sample responded predominantly to relative rather than to absolute speed. Relative speed tuning curves were similar at different center–surround velocity combinations. These relative motion-sensitive neurons in macaque area V1 probably contribute to figure/ground segmentation and motion discontinuity detection.


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