Inhibitory threshold for critical-period activation in primary visual cortex

Nature ◽  
2000 ◽  
Vol 404 (6774) ◽  
pp. 183-186 ◽  
Author(s):  
Michela Fagiolini ◽  
Takao K. Hensch
Keyword(s):  
Visual Cortex ◽  
Primary Visual Cortex ◽  
Critical Period ◽  
Inhibitory Threshold

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 Vision is required for the formation of binocular neurons prior to the classical critical period

2021 ◽  
Author(s):  
Liming Tan ◽  
Dario L. Ringach ◽  
S. Lawrence Zipursky ◽  
Joshua T. Trachtenberg
Keyword(s):  
Visual Cortex ◽  
Primary Visual Cortex ◽  
Depth Perception ◽  
Critical Period ◽  
Visual Stimuli ◽  
Cortical Responses ◽  
Eye Opening

Depth perception emerges from the development of binocular neurons in primary visual cortex. Vision is required for these neurons to acquire their mature responses to visual stimuli. A prevalent view is that vision does not influence binocular circuitry until the onset of the critical period, about a week after eye opening, and that this relies on inhibition. Here, we show that vision is required to form binocular neurons and to improve binocular tuning and matching from eye opening until critical period closure. Inhibition is not required for this process, but rather antagonizes it. Vision improves the tuning properties of binocular neurons by strengthening and sharpening ipsilateral eye cortical responses. This progressively changes the population of neurons in the binocular pool and this plasticity is sensitive to interocular differences prior to the critical period. Thus, vision guides binocular plasticity from eye opening and prior to the classically defined critical period.

Age-Dependent Decline in Supragranular Long-Term Synaptic Plasticity by Increased Inhibition During the Critical Period in the Rat Primary Visual Cortex

2009 ◽  
Vol 101 (1) ◽  
pp. 269-275 ◽  
Author(s):  
Hyun-Jong Jang ◽  
Kwang-Hyun Cho ◽  
Hyun-Sok Kim ◽  
Sang June Hahn ◽  
Myung-Suk Kim ◽  
...  
Keyword(s):  
Synaptic Plasticity ◽  
Visual Cortex ◽  
Primary Visual Cortex ◽  
Critical Period ◽  
Excitatory Postsynaptic Potential ◽  
Age Dependent ◽  
Layer 4 ◽  
Old Rats ◽  
Synaptic Model

Supragranular long-term potentiation (LTP) and depression (LTD) are continuously induced in the pathway from layer 4 during the critical period in the rodent primary visual cortex, which limits the use of supragranular long-term synaptic plasticity as a synaptic model for the mechanism of ocular dominance (OD) plasticity. The results of the present study demonstrate that the pulse duration of extracellular stimulation to evoke a field potential (FP) is critical to induction of LTP and LTD in this pathway. LTP and LTD were induced in the pathway from layer 4 to layer 2/3 in slices from 3-wk-old rats when FPs were evoked by 0.1- and 0.2-ms pulses. LTP and LTD were induced in slices from 5-wk-old rats when evoked by stimulation with a 0.2-ms pulse but not by stimulation with a 0.1-ms pulse. Both the inhibitory component of FP and the inhibitory/excitatory postsynaptic potential amplitude ratio evoked by stimulation with a 0.1-ms pulse were greater than the values elicited by a 0.2-ms pulse. Stimulation with a 0.1-ms pulse at various intensities that showed the similar inhibitory FP component with the 0.2-ms pulse induced both LTD and LTP in 5-wk-old rats. Thus extracellular stimulation with shorter-duration pulses at higher intensity resulted in greater inhibition than that observed with longer-duration pulses at low intensity. This increased inhibition might be involved in the age-dependent decline of synaptic plasticity during the critical period. These results provide an alternative synaptic model for the mechanism of OD plasticity.

scholarly journals Closing the Critical Period Is Required for the Maturation of Binocular Integration in Mouse Primary Visual Cortex

2021 ◽  
Vol 15 ◽  
Author(s):  
Jiangping Chan ◽  
Xiangwen Hao ◽  
Qiong Liu ◽  
Jianhua Cang ◽  
Yu Gu
Keyword(s):  
Visual Cortex ◽  
Mouse Model ◽  
Primary Visual Cortex ◽  
Depth Perception ◽  
Critical Period ◽  
Visual Experience ◽  
Extracellular Recording ◽  
Molecular Assay ◽  
Binocular Matching

Binocular matching of orientation preference between the two eyes is a common form of binocular integration that is regarded as the basis for stereopsis. How critical period plasticity enables binocular matching under the guidance of normal visual experience has not been fully demonstrated. To investigate how critical period closure affects the binocular matching, a critical period prolonged mouse model was constructed through the administration of bumetanide, an NKCC1 transporter antagonist. Using acute in vivo extracellular recording and molecular assay, we revealed that binocular matching was transiently disrupted due to heightened plasticity after the normal critical period, together with an increase in the density of spines and synapses, and the upregulation of GluA1 expression. Diazepam (DZ)/[(R, S)-3-(2-carboxypiperazin-4-yl) propyl-1-phosphonic acid (CPP)] could reclose the extended critical period, and rescue the deficits in binocular matching. Furthermore, the extended critical period, alone, with normal visual experience is sufficient for the completion of binocular matching in amblyopic mice. Similarly, prolonging the critical period into adulthood by knocking out Nogo-66 receptor can prevent the normal maturation of binocular matching and depth perception. These results suggest that maintaining an optimal plasticity level during adolescence is most beneficial for the systemic maturation. Extending the critical period provides new clues for the maturation of binocular vision and may have critical implications for the treatment of amblyopia.

scholarly journals MeCP2 regulates the timing of critical period plasticity that shapes functional connectivity in primary visual cortex

2015 ◽  
Vol 112 (34) ◽  
pp. E4782-E4791 ◽  
Author(s):  
Keerthi Krishnan ◽  
Bor-Shuen Wang ◽  
Jiangteng Lu ◽  
Lang Wang ◽  
Arianna Maffei ◽  
...  
Keyword(s):  
Visual Cortex ◽  
Primary Visual Cortex ◽  
Critical Period ◽  
Cortical Cell ◽  
Autism Spectrum ◽  
Developmental Trajectory ◽  
Critical Periods ◽  
Functional Deficits ◽  
Inhibitory Circuitry ◽  
Gaba Transmission

Mutations in methyl-CpG-binding protein 2 (MeCP2) cause Rett syndrome, an autism spectrum-associated disorder with a host of neurological and sensory symptoms, but the pathogenic mechanisms remain elusive. Neuronal circuits are shaped by experience during critical periods of heightened plasticity. The maturation of cortical GABA inhibitory circuitry, the parvalbumin+(PV+) fast-spiking interneurons in particular, is a key component that regulates the initiation and termination of the critical period. UsingMeCP2-nullmice, we examined experience-dependent development of neural circuits in the primary visual cortex. The functional maturation of parvalbumin interneurons was accelerated upon vision onset, as indicated by elevated GABA synthetic enzymes, vesicular GABA transporter, perineuronal nets, and enhanced GABA transmission among PV interneurons. These changes correlated with a precocious onset and closure of critical period and deficient binocular visual function in mature animals. Reduction of GAD67 expression rescued the precocious opening of the critical period, suggesting its major role in MECP2-mediated regulation of experience-driven circuit development. Our results identify molecular changes in a defined cortical cell type and link aberrant developmental trajectory to functional deficits in a model of neuropsychiatric disorder.

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

2019 ◽  
Vol 116 (43) ◽  
pp. 21812-21820 ◽  
Author(s):  
Yujiao Jennifer Sun ◽  
J. Sebastian Espinosa ◽  
Mahmood S. Hoseini ◽  
Michael P. Stryker
Keyword(s):  
Visual Cortex ◽  
Primary Visual Cortex ◽  
Critical Period ◽  
Molecular Mechanisms ◽  
Visual Experience ◽  
Structural Basis ◽  
Visual Responses ◽  
Functional Changes ◽  
Anatomical Changes ◽  
Layer 2

The 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 d. These findings reveal intracortical anatomical changes in cellular layers of the cortex that can account for rapid activity-dependent plasticity.

scholarly journals Activation of NMDA Receptors Is Necessary for the Recovery of Cortical Binocularity

2010 ◽  
Vol 103 (5) ◽  
pp. 2700-2706 ◽  
Author(s):  
Thomas E. Krahe ◽  
Alexandre E. Medina
Keyword(s):  
Visual Cortex ◽  
Primary Visual Cortex ◽  
Binocular Vision ◽  
Critical Period ◽  
Functional Change ◽  
Monocular Deprivation ◽  
Extracellular Recordings ◽  
Aspartate Receptor ◽  
Critical Period Of Development

Classic experiments have indicated that monocular deprivation (MD) for a few days during a critical period of development results in a decrease in the strength of connections mediating responses to the deprived eye, leading to a dramatic breakdown of cortical neuron binocularity. Despite the substantial functional change in the visual cortex, recovery from the effects of MD can be obtained if binocular vision is promptly restored. While great efforts have been made to elucidate the mechanisms regulating loss of deprived eye function, the mechanisms that underlie the recovery of cortical binocularity are poorly understood. Here, we examined whether activation of the N-methyl-d-aspartate receptor (NMDAR) is required for the recovery of cortical binocularity by pharmacologically blocking the NMDAR using d,l-2-amino-5-phosphonopentanoic (APV). Ferrets ( n = 10) were monocularly deprived for 6 days, and osmotic minipumps, filled with APV (5.6 mg/ml) or saline, were surgically implanted into the primary visual cortex. One day after surgery, the deprived eye was reopened, and the animals were allowed 24 h of binocular vision. Extracellular recordings showed that intracortical infusion of the NMDAR antagonist, APV, prevented recovery of cortical binocularity while preserving neuronal responsiveness. These findings provide an important new insight for a specific role of NMDARs in the recovery of cortical binocularity from the effects of MD.

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