Hebbian Plasticity and Homeostasis in a Model of Hypercolumn of the Visual Cortex

2010 ◽  
Vol 22 (7) ◽  
pp. 1837-1859 ◽  
Author(s):  
R. Rossi Pool ◽  
G. Mato

Neurons in the nervous system display a wide variety of plasticity processes. Among them are covariance-based rules and homeostatic plasticity. By themselves, the first ones tend to generate instabilities because of the unbounded potentiation of synapses. The second ones tend to stabilize the system by setting a target for the postsynaptic firing rate. In this work, we analyze the combined effect of these two mechanisms in a simple model of hypercolumn of the visual cortex. We find that the presence of homeostatic plasticity together with nonplastic uniform inhibition stabilizes the effect of Hebbian plasticity. The system can reach nontrivial solutions, where the recurrent intracortical connections are strongly modulated. The modulation is strong enough to generate contrast invariance. Moreover, this state can be reached even beginning from a weakly modulated initial condition.

2017 ◽  
Vol 372 (1715) ◽  
pp. 20160155 ◽  
Author(s):  
Ada X. Yee ◽  
Yu-Tien Hsu ◽  
Lu Chen

Hebbian and homeostatic plasticity are two major forms of plasticity in the nervous system: Hebbian plasticity provides a synaptic basis for associative learning, whereas homeostatic plasticity serves to stabilize network activity. While achieving seemingly very different goals, these two types of plasticity interact functionally through overlapping elements in their respective mechanisms. Here, we review studies conducted in the mammalian central nervous system, summarize known circuit and molecular mechanisms of homeostatic plasticity, and compare these mechanisms with those that mediate Hebbian plasticity. We end with a discussion of ‘local’ homeostatic plasticity and the potential role of local homeostatic plasticity as a form of metaplasticity that modulates a neuron's future capacity for Hebbian plasticity. This article is part of the themed issue ‘Integrating Hebbian and homeostatic plasticity’.


2019 ◽  
Author(s):  
Alejandro Torrado Pacheco ◽  
Juliet Bottorff ◽  
Gina G. Turrigiano

SUMMARYHomeostatic plasticity is hypothesized to regulate neuronal activity around a stable set point to compensate for learning-related plasticity. This regulation is predicted to be bidirectional but only upward firing rate homeostasis (FRH) has been demonstrated in vivo. We combined chronic electrophysiology in freely behaving animals with a protocol that induces robust plasticity in primary visual cortex (V1) to induce downward FRH and show that neurons bidirectionally regulate firing rates around an individual set point. Downward FRH did not require N-methyl-D-aspartate receptor (NMDAR) signaling and was associated with homeostatic scaling down of synaptic strengths. Like upward FRH, downward FRH was gated by vigilance state, but in the opposite direction: it occurred during sleep and not during wake. In contrast, FR changes associated with Hebbian plasticity happened independently of sleep and wake. Thus, we find that sleep’s impact on neuronal plasticity depends on the particular forms of plasticity that are engaged.


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’.


1994 ◽  
Vol 72 (3) ◽  
pp. 1220-1226 ◽  
Author(s):  
D. Czepita ◽  
S. N. Reid ◽  
N. W. Daw

1. Cats were reared in the dark to 3, 5, and 11 mo. We studied the N-methyl-D-aspartate (NMDA) receptor contribution to the visual response in the cortex, defined as the percentage reduction in visual response after application of 2-amino-5-phosphonovaleric acid (APV). We also studied the firing rate in response to the optimal visual stimulus and the spontaneous activity. We made comparisons of all these properties between light-reared and dark-reared animals. 2. The NMDA receptor contribution to the visual response in layers IV, V, and VI of dark-reared animals was substantially above that in light-reared animals at all ages tested. 3. The specificity of receptive field properties in dark-reared animals showed some degeneration between 6 wk and 3 mo of age. At > or = 3 mo, almost no cells were specific for orientation and direction of movement. 4. Firing rate was lower in dark-reared animals at all ages, suggesting a decrease in excitatory drive to the visual cortex. 5. Spontaneous activity was equal in dark- and light-reared animals, suggesting that the overall level of activity (including visual responses as well as spontaneous activity) in light-reared animals is higher than in dark-reared animals. This should tend to upregulate glutamate receptors in general in dark-reared animals.


Author(s):  
Gordon M. Shepherd ◽  
Michele Migliore ◽  
Francesco Cavarretta

The olfactory bulb is the site of the first synaptic processing of the olfactory input from the nose. It is present in all vertebrates (except cetaceans) and a the analogous antennal lobe in most invertebrates. With its sharply demarcated cell types and histological layers, and some well-studied synaptic interactions, it is one of the first and clearest examples of the microcircuit concept in the central nervous system. The olfactory bulb microcircuit receives the information in the sensory domain and transforms it into information in the neural domain. Traditionally, it has been considered analogous to the retina in processing its sensory input, but that has been replaced by the view that it is more similar to the thalamus or primary visual cortex in processing its multidimensional input. This chapter describes the main synaptic connections and functional operations and how they provide the output to the olfactory cortex


2004 ◽  
Vol 21 (4) ◽  
pp. 653-670 ◽  
Author(s):  
KATHRYN M. MURPHY ◽  
KEVIN R. DUFFY ◽  
DAVID G. JONES

When normal binocular visual experience is disrupted during postnatal development, it affects the maturation of cortical circuits and often results in the development of poor visual acuity known as amblyopia. Two main factors contribute to the development of amblyopia: visual deprivation and reduced binocular competition. We investigated the affect of these two amblyogenic factors on the expression of the NMDAR1 subunit in the visual cortex because activation of the NMDA receptor is a key mechanism of developmental neural plasticity. We found that disruption of binocular correlations by monocular deprivation promoted a topographic loss of NMDAR1 expression within the cortical representations of the central visual field and the vertical and horizontal meridians. In contrast, binocular deprivation, which primarily affects visual deprivation, promoted an increase in NMDAR1 expression throughout the visual cortex. These different changes in NMDAR1 expression can be described as topographic and homeostatic plasticity of NMDA expression, respectively. In addition, the changes in NMDA expression in the visual cortex provide a greater understanding of the neural mechanisms that underlie the development of amblyopia and the potential for visual recovery.


2004 ◽  
Vol 5 (2) ◽  
pp. 97-107 ◽  
Author(s):  
Gina G. Turrigiano ◽  
Sacha B. Nelson

2012 ◽  
Vol 2012 ◽  
pp. 1-10 ◽  
Author(s):  
José Fernando Maya-Vetencourt ◽  
Laura Baroncelli ◽  
Alessandro Viegi ◽  
Ettore Tiraboschi ◽  
Eero Castren ◽  
...  

The central nervous system architecture is markedly modified by sensory experience during early life, but a decline of plasticity occurs with age. Recent studies have challenged this dogma providing evidence that both pharmacological treatments and paradigms based on the manipulation of environmental stimulation levels can be successfully employed as strategies for enhancing plasticity in the adult nervous system. Insulin-like growth factor 1 (IGF-1) is a peptide implicated in prenatal and postnatal phases of brain development such as neurogenesis, neuronal differentiation, synaptogenesis, and experience-dependent plasticity. Here, using the visual system as a paradigmatic model, we report that IGF-1 reactivates neural plasticity in the adult brain. Exogenous administration of IGF-1 in the adult visual cortex, indeed, restores the susceptibility of cortical neurons to monocular deprivation and promotes the recovery of normal visual functions in adult amblyopic animals. These effects were accompanied by a marked reduction of intracortical GABA levels. Moreover, we show that a transitory increase of IGF-1 expression is associated to the plasticity reinstatement induced by environmental enrichment (EE) and that blocking IGF-1 action by means of the IGF-1 receptor antagonist JB1 prevents EE effects on plasticity processes.


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