Behavioural Recovery from Visual Deprivation: Comments on the Critical Period

1979 ◽  
pp. 149-160 ◽  
Author(s):  
Brian Timney ◽  
Donald E. Mitchell
Keyword(s):  
Critical Period ◽  
Visual Deprivation

scholarly journals Visual Deprivation During the Critical Period Enhances Layer 2/3 GABAergic Inhibition in Mouse V1

2016 ◽  
Vol 36 (22) ◽  
pp. 5914-5919 ◽  
Author(s):  
Madhuvanthi Kannan ◽  
Garrett G. Gross ◽  
Don B. Arnold ◽  
Michael J. Higley
Keyword(s):  
Critical Period ◽  
Visual Deprivation ◽  
Gabaergic Inhibition ◽  
Layer 2

scholarly journals Developmental switch in the polarity of experience-dependent synaptic changes in layer 6 of mouse visual cortex

2011 ◽  
Vol 106 (5) ◽  
pp. 2499-2505 ◽  
Author(s):  
Emily Petrus ◽  
Terence T. Anguh ◽  
Huy Pho ◽  
Angela Lee ◽  
Nicholas Gammon ◽  
...  
Keyword(s):  
Visual Cortex ◽  
Critical Period ◽  
Pyramidal Neurons ◽  
Light Exposure ◽  
Visual Deprivation ◽  
Thalamic Reticular Nucleus ◽  
Reticular Nucleus ◽  
Excitatory Synapses ◽  
Thalamic Nuclei ◽  
Developmental Age

Layer 6 (L6) of primary sensory cortices is distinct from other layers in that it provides a major cortical input to primary sensory thalamic nuclei. L6 pyramidal neurons in the primary visual cortex (V1) send projections to the lateral geniculate nucleus (LGN), as well as to the thalamic reticular nucleus and higher order thalamic nuclei. Although L6 neurons are proposed to modulate the activity of thalamic relay neurons, how sensory experience regulates L6 neurons is largely unknown. Several days of visual deprivation homeostatically adjusts excitatory synapses in L4 and L2/3 of V1 depending on the developmental age. For instance, L4 exhibits an early critical period during which visual deprivation homeostatically scales up excitatory synaptic transmission. On the other hand, homeostatic changes in L2/3 excitatory synapses are delayed and persist into adulthood. In the present study we examined how visual deprivation affects excitatory synapses on L6 pyramidal neurons. We found that L6 pyramidal neurons homeostatically increase the strength of excitatory synapses following 2 days of dark exposure (DE), which was readily reversed by 1 day of light exposure. This effect was restricted to an early critical period, similar to that reported for L4 neurons. However, at a later developmental age, a longer duration of DE (1 wk) decreased the strength of excitatory synapses, which reversed to normal levels with light exposure. These changes are opposite to what is predicted from the homeostatic plasticity theory. Our results suggest that L6 neurons differentially adjust their excitatory synaptic strength to visual deprivation depending on the age of the animals.

scholarly journals Synaptic plasticity onto inhibitory neurons as a mechanism for ocular dominance plasticity

2018 ◽  
Author(s):  
Jacopo Bono ◽  
Claudia Clopath
Keyword(s):  
Synaptic Plasticity ◽  
Critical Period ◽  
Ocular Dominance ◽  
Visual Deprivation ◽  
Inhibitory Neurons ◽  
Cortical Circuits ◽  
Ocular Dominance Plasticity ◽  
Opening And Closing ◽  
Recent Experimental Work ◽  
Cortical Maturation

AbstractOcular dominance plasticity is a well-documented phenomenon allowing us to study properties of cortical maturation. Understanding this maturation might be an important step towards unravelling how cortical circuits function. However, it is still not fully understood which mechanisms are responsible for the opening and closing of the critical period for ocular dominance and how changes in cortical responsiveness arise after visual deprivation. In this article, we present a theory of ocular dominance plasticity. Following recent experimental work, we propose a framework where a reduction in inhibition is necessary for ocular dominance plasticity in both juvenile and adult animals. In this framework, two ingredients are crucial to observe ocular dominance shifts: a sufficient level of inhibition as well as excitatory-to-inhibitory synaptic plasticity. In our model, the former is responsible for the opening of the critical period, while the latter limits the plasticity in adult animals. Finally, we also provide a possible explanation for the variability in ocular dominance shifts observed in individual neurons and for the counter-intuitive shifts towards the closed eye.

Pioneers of cortical plasticity: six classic papers by Wiesel and Hubel

2008 ◽  
Vol 99 (6) ◽  
pp. 2741-2744 ◽  
Author(s):  
Martha Constantine-Paton
Keyword(s):  
Critical Period ◽  
Striate Cortex ◽  
Cortical Plasticity ◽  
Receptive Fields ◽  
Lateral Geniculate Body ◽  
Visual Deprivation ◽  
Cell Responses ◽  
Single Cell Responses ◽  
Eye Closure ◽  
Classic Papers

This essay looks at six APS classic papers published by D. H. Hubel and T. N. Wiesel that first identified a developmental critical period for environment influenced receptive field plasticity in the visual pathway. These classic papers are freely available online. These are listed here, in chronological order. Wiesel TN, Hubel DH. Effects of visual deprivation on morphology and physiology of cells in the cat's lateral geniculate body. J Neurophysiol 26: 978–993, 1963 ( http://jn.physiology.org/cgi/reprint/26/6/978 ). Hubel DH, Wiesel TN. Receptive fields of cells in striate cortex of very young, visually inexperienced kittens. J Neurophysiol 26: 994–1002, 1963 ( http://jn.physiology.org/cgi/reprint/26/6/994 ). Wiesel TN, Hubel DH. Single-cell responses in striate cortex of kittens deprived of vision in one eye. J Neurophysiol 26: 1003–1017, 1963 ( http://jn.physiology.org/cgi/reprint/26/6/1003 ). Wiesel TN, Hubel DH. Comparison of the effects of unilateral and bilateral eye closure on cortical unit responses in kittens. J Neurophysiol 28: 1029–1040, 1965 ( http://jn.physiology.org/cgi/reprint/28/6/1029 ). Hubel DH, Wiesel TN. Binocular interaction in striate cortex of kittens reared with artificial squint. J Neurophysiol 28: 1041–1059, 1965 ( http://jn.physiology.org/cgi/reprint/28/6/1041 ). Wiesel TN, Hubel DH. Extent of recovery from the effects of visual deprivation in kittens. J Neurophysiol 28: 1060–1072, 1965 ( http://jn.physiology.org/cgi/reprint/28/6/1060 ).

Visual Experience Is Necessary for Maintenance But Not Development of Receptive Fields in Superior Colliculus

2005 ◽  
Vol 94 (3) ◽  
pp. 1962-1970 ◽  
Author(s):  
M. M. Carrasco ◽  
K. A. Razak ◽  
S. L. Pallas
Keyword(s):  
Superior Colliculus ◽  
Critical Period ◽  
Visual Experience ◽  
Sensory Deprivation ◽  
Receptive Fields ◽  
Visual Deprivation ◽  
Visual Development ◽  
Retinotopic Maps ◽  
Nmda Receptor Blockade ◽  
Dark Rearing

Sensory deprivation is thought to have an adverse effect on visual development and to prolong the critical period for plasticity. Once the animal reaches adulthood, however, synaptic connectivity is understood to be largely stable. We reported previously that N-methyl-d-aspartate (NMDA) receptor blockade in the superior colliculus of the Syrian hamster prevents refinement of receptive fields (RFs) in normal or compressed retinotopic projections, resulting in target neurons with enlarged RFs but normal stimulus tuning. Here we asked whether visually driven activity is necessary for refinement or maintenance of retinotopic maps or if spontaneous activity is sufficient. Animals were deprived of light either in adulthood only or from birth until the time of recording. We found that dark rearing from birth to 2 mo of age had no effect on the timing and extent of RF refinement as assessed with single unit extracellular recordings. Visual deprivation in adulthood also had no effect. Continuous dark rearing from birth into adulthood, however, resulted in a progressive loss of refinement, resulting in enlarged, asymmetric receptive fields and altered surround suppression in adulthood. Thus unlike in visual cortex, early visually driven activity is not necessary for refinement of receptive fields during development, but is required to maintain refined visual projections in adulthood. Because the map can refine normally in the dark, these results argue against a deprivation-induced delay in critical period closure, and suggest instead that early visual deprivation leaves target neurons more vulnerable to deprivation that continues after refinement.

scholarly journals Changes in input strength and number are driven by distinct mechanisms at the retinogeniculate synapse

2014 ◽  
Vol 112 (4) ◽  
pp. 942-950 ◽  
Author(s):  
David J. Lin ◽  
Erin Kang ◽  
Chinfei Chen
Keyword(s):  
Critical Period ◽  
Visual Experience ◽  
Ganglion Cells ◽  
Visual Deprivation ◽  
Homeostatic Plasticity ◽  
Dorsal Lateral Geniculate Nucleus ◽  
Relay Neuron ◽  
Retinogeniculate Synapse ◽  
Dorsal Lateral Geniculate ◽  
Relay Neurons

Recent studies have demonstrated that vision influences the functional remodeling of the mouse retinogeniculate synapse, the connection between retinal ganglion cells and thalamic relay neurons in the dorsal lateral geniculate nucleus (LGN). Initially, each relay neuron receives a large number of weak retinal inputs. Over a 2- to 3-wk developmental window, the majority of these inputs are eliminated, and the remaining inputs are strengthened. This period of refinement is followed by a critical period when visual experience changes the strength and connectivity of the retinogeniculate synapse. Visual deprivation of mice by dark rearing from postnatal day (P)20 results in a dramatic weakening of synaptic strength and recruitment of additional inputs. In the present study we asked whether experience-dependent plasticity at the retinogeniculate synapse represents a homeostatic response to changing visual environment. We found that visual experience starting at P20 following visual deprivation from birth results in weakening of existing retinal inputs onto relay neurons without significant changes in input number, consistent with homeostatic synaptic scaling of retinal inputs. On the other hand, the recruitment of new inputs to the retinogeniculate synapse requires previous visual experience prior to the critical period. Taken together, these findings suggest that diverse forms of homeostatic plasticity drive experience-dependent remodeling at the retinogeniculate synapse.

scholarly journals Light reintroduction after dark exposure reactivates plasticity in adults via perisynaptic activation of MMP-9

eLife ◽  
2017 ◽  
Vol 6 ◽  
Author(s):  
Sachiko Murase ◽  
Crystal L Lantz ◽  
Elizabeth M Quinlan
Keyword(s):  
Critical Period ◽  
Adult Mouse ◽  
Ocular Dominance ◽  
Visual Deprivation ◽  
Monocular Deprivation ◽  
Genetic Ablation ◽  
Dark Exposure ◽  
Cortical Synapses ◽  
Mouse Visual Cortex ◽  
Metalloproteinase 9

The sensitivity of ocular dominance to regulation by monocular deprivation is the canonical model of plasticity confined to a critical period. However, we have previously shown that visual deprivation through dark exposure (DE) reactivates critical period plasticity in adults. Previous work assumed that the elimination of visual input was sufficient to enhance plasticity in the adult mouse visual cortex. In contrast, here we show that light reintroduction (LRx) after DE is responsible for the reactivation of plasticity. LRx triggers degradation of the ECM, which is blocked by pharmacological inhibition or genetic ablation of matrix metalloproteinase-9 (MMP-9). LRx induces an increase in MMP-9 activity that is perisynaptic and enriched at thalamo-cortical synapses. The reactivation of plasticity by LRx is absent in Mmp9−/− mice, and is rescued by hyaluronidase, an enzyme that degrades core ECM components. Thus, the LRx-induced increase in MMP-9 removes constraints on structural and functional plasticity in the mature cortex.

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