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 Experience-dependent structural plasticity at pre- and postsynaptic sites of layer 2/3 cells in developing visual cortex

2019 ◽  
Author(s):  
Yujiao Jennifer Sun ◽  
J. Sebastian Espinosa ◽  
Mahmood S. Hoseini ◽  
Michael P. Stryker
Keyword(s):  
Visual Cortex ◽  
Primary Visual Cortex ◽  
Critical Period ◽  
Visual Experience ◽  
Visual Deprivation ◽  
Monocular Deprivation ◽  
Structural Basis ◽  
Dependent Plasticity ◽  
Anatomical Changes ◽  
Layer 2

AbstractThe developing brain can respond quickly to altered sensory experience by circuit reorganization. During a critical period in early life, neurons in the primary visual cortex rapidly lose responsiveness to an occluded eye and come to respond better to the open eye. While physiological and some of the molecular mechanisms of this process have been characterized, its structural basis, except for the well-known changes in the thalamocortical projection, remains obscure. To elucidate the relationship between synaptic remodeling and functional changes during this experience-dependent process, we used 2-photon microscopy to image synaptic structures of sparsely labeled layer 2/3 neurons in the binocular zone of mouse primary visual cortex. Anatomical changes at presynaptic and postsynaptic sites in mice undergoing monocular visual deprivation (MD) were compared to those in control mice with normal visual experience. We found that postsynaptic spines remodeled quickly in response to MD, with neurons more strongly dominated by the deprived eye losing more spines. These postsynaptic changes parallel changes in visual responses during MD and their recovery after restoration of binocular vision. In control animals with normal visual experience, the formation of presynaptic boutons increased during the critical period and then declined. MD affected bouton formation, but with a delay, blocking it after 3 days. These findings reveal intracortical anatomical changes in cellular layers of the cortex that can account for rapid activity-dependent plasticity.Significance statementThe operation of the cortex depends on the connections among its neurons. Taking advantage of molecular and genetic tools to label major proteins of the presynaptic and postsynaptic densities, we studied how connections of layer 2/3 excitatory neurons in mouse visual cortex were changed by monocular visual deprivation during the critical period, which causes amblyopia. The deprivation induced rapid remodeling of postsynaptic spines and impaired bouton formation. Structural measurement followed by calcium imaging demonstrated a strong correlation between changes in postsynaptic structures and functional responses in individual neurons after monocular deprivation. These findings suggest that anatomical changes at postsynaptic sites serve as a substrate for experience-dependent plasticity in the developing visual cortex.

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.

Development of Intrinsic Properties and Excitability of Layer 2/3 Pyramidal Neurons During a Critical Period for Sensory Maps in Rat Barrel Cortex

2004 ◽  
Vol 92 (1) ◽  
pp. 144-156 ◽  
Author(s):  
Miguel Maravall ◽  
Edward A. Stern ◽  
Karel Svoboda
Keyword(s):  
Critical Period ◽  
Pyramidal Neurons ◽  
Barrel Cortex ◽  
Pyramidal Cells ◽  
Membrane Properties ◽  
Sensory Maps ◽  
Layer 2 ◽  
Whole Cell Recordings ◽  
Passive Membrane Properties

The development of layer 2/3 sensory maps in rat barrel cortex (BC) is experience dependent with a critical period around postnatal days (PND) 10–14. The role of intrinsic response properties of neurons in this plasticity has not been investigated. Here we characterize the development of BC layer 2/3 intrinsic responses to identify possible sites of plasticity. Whole cell recordings were performed on pyramidal cells in acute BC slices from control and deprived rats, over ages spanning the critical period (PND 12, 14, and 17). Vibrissa trimming began at PND 9. Spiking behavior changed from phasic (more spike frequency adaptation) to regular (less adaptation) with age, such that the number of action potentials per stimulus increased. Changes in spiking properties were related to the strength of a slow Ca2+-dependent afterhyperpolarization. Maturation of the spiking properties of layer 2/3 pyramidal neurons coincided with the close of the critical period and was delayed by deprivation. Other measures of excitability, including I-f curves and passive membrane properties, were affected by development but unaffected by whisker deprivation.

scholarly journals Vision reconstructs the cellular composition of binocular circuitry during the critical period

2020 ◽  
Author(s):  
Liming Tan ◽  
Elaine Tring ◽  
Dario L. Ringach ◽  
S. Lawrence Zipursky ◽  
Joshua T. Trachtenberg
Keyword(s):  
Visual Cortex ◽  
Receptive Field ◽  
Primary Visual Cortex ◽  
Critical Period ◽  
Cellular Composition ◽  
Feature Detectors ◽  
Layer 2 ◽  
Layer 4 ◽  
High Acuity ◽  
Longitudinal Imaging

AbstractHigh acuity binocularity is established in primary visual cortex during an early postnatal critical period. In contrast to current models for the developmental of binocular neurons, we find that the binocular network present at the onset of the critical period is dismantled and remade. Using longitudinal imaging of receptive field tuning (e.g. orientation selectivity) of thousands of layer 2/3 neurons through development, we show most binocular neurons present at critical-period onset are poorly tuned and rendered monocular. These are replenished by newly formed binocular neurons that are established by a vision-dependent recruitment of well-tuned ipsilateral inputs to contralateral monocular neurons with matched tuning properties. The binocular network in layer 4 is equally unstable but does not improve. Thus, vision instructs a new and more sharply tuned binocular network in layer 2/3 by exchanging one population of neurons for another and not by refining an extant network.One Sentence SummaryUnstable binocular circuitry is transformed by vision into a network of highly tuned complex feature detectors in the cortex.

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 ).

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