scholarly journals Visual experience sculpts whole-cortex spontaneous infraslow activity patterns through an Arc-dependent mechanism

2017 ◽  
Vol 114 (46) ◽  
pp. E9952-E9961 ◽  
Author(s):  
Andrew W. Kraft ◽  
Anish Mitra ◽  
Adam Q. Bauer ◽  
Abraham Z. Snyder ◽  
Marcus E. Raichle ◽  
...  

Decades of work in experimental animals has established the importance of visual experience during critical periods for the development of normal sensory-evoked responses in the visual cortex. However, much less is known concerning the impact of early visual experience on the systems-level organization of spontaneous activity. Human resting-state fMRI has revealed that infraslow fluctuations in spontaneous activity are organized into stereotyped spatiotemporal patterns across the entire brain. Furthermore, the organization of spontaneous infraslow activity (ISA) is plastic in that it can be modulated by learning and experience, suggesting heightened sensitivity to change during critical periods. Here we used wide-field optical intrinsic signal imaging in mice to examine whole-cortex spontaneous ISA patterns. Using monocular or binocular visual deprivation, we examined the effects of critical period visual experience on the development of ISA correlation and latency patterns within and across cortical resting-state networks. Visual modification with monocular lid suturing reduced correlation between left and right cortices (homotopic correlation) within the visual network, but had little effect on internetwork correlation. In contrast, visual deprivation with binocular lid suturing resulted in increased visual homotopic correlation and increased anti-correlation between the visual network and several extravisual networks, suggesting cross-modal plasticity. These network-level changes were markedly attenuated in mice with genetic deletion of Arc, a gene known to be critical for activity-dependent synaptic plasticity. Taken together, our results suggest that critical period visual experience induces global changes in spontaneous ISA relationships, both within the visual network and across networks, through an Arc-dependent mechanism.

Weed Science ◽  
1995 ◽  
Vol 43 (4) ◽  
pp. 634-639 ◽  
Author(s):  
Claudio M. Dunan ◽  
Philip Westra ◽  
Edward E. Schweizer ◽  
Donald W. Lybecker ◽  
Frank D. Moore

The question of when to control weeds traditionally has been approached with the calculation of critical periods (CP) based on crop yields. The concept of economic critical period (ECP) and early (EEPT) and late (LEFT) economic period thresholds are presented as a comprehensive approach to answer the same question based on economic losses and costs of control. ECP is defined as the period when the benefit of controlling weeds is greater than its cost. EEPT and LEFT are the limits of the ECP and can be used to determine when first and last weed control measures should be performed. Calculation of EEPT accounts for the economic losses due to weed competition that occur between planting and postemergence weed control. In this way it is possible to better evaluate the economic feasibility of using preplant or preemergence control tactics. The EEPT for DCPA application is analyzed in the context of onion production in Colorado. The EEPT for DCPA application was calculated from an empirical regression model that assessed the impact of weed load and time of weed removal on onion yields. The EEPT was affected by control efficacy, weed-free yield, DCPA cost, and onion price. DCPA application was economically advisable in only one of 20 fields analyzed because of the tow DCPA efficacy (60%).


2019 ◽  
Vol 44 (12) ◽  
pp. 1386-1392
Author(s):  
Hongmei Shi ◽  
Yanming Wang ◽  
Xuemei Liu ◽  
Lin Xia ◽  
Yao Chen ◽  
...  

2020 ◽  
Vol 117 (38) ◽  
pp. 23242-23251 ◽  
Author(s):  
Rebecca K. Reh ◽  
Brian G. Dias ◽  
Charles A. Nelson ◽  
Daniela Kaufer ◽  
Janet F. Werker ◽  
...  

Brain plasticity is dynamically regulated across the life span, peaking during windows of early life. Typically assessed in the physiological range of milliseconds (real time), these trajectories are also influenced on the longer timescales of developmental time (nurture) and evolutionary time (nature), which shape neural architectures that support plasticity. Properly sequenced critical periods of circuit refinement build up complex cognitive functions, such as language, from more primary modalities. Here, we consider recent progress in the biological basis of critical periods as a unifying rubric for understanding plasticity across multiple timescales. Notably, the maturation of parvalbumin-positive (PV) inhibitory neurons is pivotal. These fast-spiking cells generate gamma oscillations associated with critical period plasticity, are sensitive to circadian gene manipulation, emerge at different rates across brain regions, acquire perineuronal nets with age, and may be influenced by epigenetic factors over generations. These features provide further novel insight into the impact of early adversity and neurodevelopmental risk factors for mental disorders.


2005 ◽  
Vol 94 (3) ◽  
pp. 1962-1970 ◽  
Author(s):  
M. M. Carrasco ◽  
K. A. Razak ◽  
S. L. Pallas

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.


2014 ◽  
Vol 112 (4) ◽  
pp. 942-950 ◽  
Author(s):  
David J. Lin ◽  
Erin Kang ◽  
Chinfei Chen

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.


2018 ◽  
Author(s):  
Adema Ribic ◽  
Michael C. Crair ◽  
Thomas Biederer

HighlightsThe synaptogenic molecule SynCAM 1 is selectively regulated by visual experienceSynCAM 1 controls thalamic input onto cortical Parvalbumin (PV+) interneuronsPV+-specific knockdown of SynCAM 1 arrests maturation of cortical inhibitionThalamic excitation onto PV+ interneurons is essential for critical period closureeTOC BlurbRibic et al. show that network plasticity in both young and adult cortex is restricted by the synapse organizing molecule SynCAM 1. On a cellular level, it functions in Parvalbumin-positive interneurons to recruit thalamocortical terminals. This controls the maturation of inhibitory drive and restricts plasticity in the cortex. These results reveal the synaptic locus of cortical plasticity and identify the first cell-autonomous synaptic factor for closure of cortical critical periods.SummaryBrain plasticity peaks early in life and tapers in adulthood. This is exemplified in the primary visual cortex, where brief loss of vision to one eye abrogates cortical responses to inputs from that eye during the critical period, but not in adulthood. The synaptic locus of critical period plasticity and the cell-autonomous synaptic factors timing these periods remain unclear. We here demonstrate that the immunoglobulin protein Synaptic Cell Adhesion Molecule 1 (SynCAM 1/Cadm1) is regulated by visual experience and limits visual cortex plasticity. SynCAM 1 selectively controls the number of excitatory thalamocortical (TC) inputs onto Parvalbumin (PV+) interneurons and loss of SynCAM 1 in turn impairs the maturation of TC-driven feed-forward inhibition. SynCAM 1 acts in cortical PV+ interneurons to perform these functions and its PV+-specific knockdown prevents the age-related plasticity decline. These results identify a synapse type-specific, cell-autonomous mechanism that governs circuit maturation and closes the visual critical period.


2009 ◽  
Vol 101 (2) ◽  
pp. 855-861 ◽  
Author(s):  
Joshua Faguet ◽  
Bruno Maranhao ◽  
Spencer L. Smith ◽  
Joshua T. Trachtenberg

In the cerebral cortex, neuronal circuits are first laid down by intrinsic mechanisms and then refined by experience. In the canonical model, this refinement is driven by activity-dependent competition between inputs for some limited cortical resource. Here we examine this idea in the mouse visual cortex at the peak of the critical period for experience-dependent plasticity. By imaging intrinsic optical responses, we mapped the strength and size of each eye's cortical representation in normal mice, mice that had been deprived of patterned vision uni- or bilaterally, and in mice in which the contralateral eye had been removed. We find that for both eyes, a period of visual deprivation results in a loss of cortical responsiveness to stimulation through the deprived eye. In addition, the ipsilateral eye pathway is affected by the quality of vision through the opposite eye. Our findings indicate that although both contra- and ipsilateral eye pathways require visual experience for their maintenance, ipsilateral eye projections bear an additional, unique sensitivity to binocular interactions.


2018 ◽  
Author(s):  
David B. Mudd ◽  
Timothy S. Balmer ◽  
So Yeon Kim ◽  
Noura Machhour ◽  
Sarah L. Pallas

AbstractDuring a critical period in development, spontaneous and evoked retinal activity shape visual pathways in an adaptive fashion. Interestingly, spontaneous activity is sufficient for spatial refinement of visual receptive fields in superior colliculus (SC) and visual cortex (V1), but early visual experience is necessary to maintain inhibitory synapses and stabilize RFs in adulthood (Carrasco et al. 2005, 2011; Carrasco & Pallas 2006; Balmer & Pallas 2015a). In visual cortex (V1), brain-derived neurotrophic factor (BDNF) and its high affinity receptor TrkB are important for development of visual acuity, inhibition, and regulation of the critical period for ocular dominance plasticity (Hanover et al., 1999; Huang et al., 1999; Gianfranceschi et al., 2003). To examine the generality of this signaling pathway for visual system plasticity, the present study examined the role of TrkB signaling during the critical period for RF refinement in SC. Activating TrkB receptors during the critical period (P33-40) in DR subjects produced normally refined RFs, and blocking TrkB receptors in light-exposed animals resulted in enlarged adult RFs like those in DR animals. We also report here that deprivation- or TrkB blockade-induced RF enlargement in adulthood impaired fear responses to looming overhead stimuli, and negatively impacted visual acuity. Thus, early TrkB activation is both necessary and sufficient to maintain visual RF refinement, robust looming responses, and visual acuity in adulthood. These findings suggest a common signaling pathway exists for the maturation of inhibition between V1 and SC.Significance StatementReceptive field refinement in superior colliculus (SC) differs from more commonly studied examples of critical period plasticity in visual pathways in that it does not require visual experience to occur; rather spontaneous activity is sufficient. Maintenance of refinement beyond puberty requires a brief, early exposure to light in order to stabilize the lateral inhibition that shapes receptive fields. We find that TrkB activation during a critical period can substitute for visual experience in maintaining receptive field refinement into adulthood, and that this maintenance is beneficial to visual survival behaviors. Thus, as in some other types of plasticity, TrkB signaling plays a crucial role in RF refinement.


2020 ◽  
Vol 2020 ◽  
pp. 1-10
Author(s):  
Milo R. Smith ◽  
Priscilla Yevoo ◽  
Masato Sadahiro ◽  
Ben Readhead ◽  
Brian Kidd ◽  
...  

The tens of thousands of industrial and synthetic chemicals released into the environment have an unknown but potentially significant capacity to interfere with neurodevelopment. Consequently, there is an urgent need for systematic approaches that can identify disruptive chemicals. Little is known about the impact of environmental chemicals on critical periods of developmental neuroplasticity, in large part, due to the challenge of screening thousands of chemicals. Using an integrative bioinformatics approach, we systematically scanned 2001 environmental chemicals and identified 50 chemicals that consistently dysregulate two transcriptional signatures of critical period plasticity. These chemicals included pesticides (e.g., pyridaben), antimicrobials (e.g., bacitracin), metals (e.g., mercury), anesthetics (e.g., halothane), and other chemicals and mixtures (e.g., vehicle emissions). Application of a chemogenomic enrichment analysis and hierarchical clustering across these diverse chemicals identified two clusters of chemicals with one that mimicked an immune response to pathogen, implicating inflammatory pathways and microglia as a common chemically induced neuropathological process. Thus, we established an integrative bioinformatics approach to systematically scan thousands of environmental chemicals for their ability to dysregulate molecular signatures relevant to critical periods of development.


2019 ◽  
Author(s):  
Yujiao Jennifer Sun ◽  
J. Sebastian Espinosa ◽  
Mahmood S. Hoseini ◽  
Michael P. Stryker

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.


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