Gene expression patterns during enhanced periods of visual cortex plasticity

Prasad, Shiv S.; Kojic, Luba; Li, P; Mitchell, Donald E.; Hachisuka, Akiko; Sawada, J-I; Gu, Qiang; Cynader, Max S.

doi:10.1016/s0306-4522(01)00570-x

Cited by 37 publications

(29 citation statements)

References 34 publications

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“…Rather, vision is required to set the stage for later retinogeniculate plasticity. These results are consistent with a model in which the onset of visual experience initiates expression of a particular genetic program that permits plasticity within visual system neurons (Prasad et al, 2002;Majdan and Shatz, 2006;Tropea et al, 2006). Without triggering of this genetic program, as in chronic deprivation, a different set of genes is expressed that prohibit synaptic adaptation to the external environment.…”

Section: Discussionsupporting

confidence: 88%

Vision Triggers an Experience-Dependent Sensitive Period at the Retinogeniculate Synapse

Hooks

Chen²

2008

J. Neurosci.

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In the mammalian visual system, sensory experience is widely thought to sculpt cortical circuits during a precise critical period. In contrast, subcortical regions, such as the thalamus, were thought to develop at earlier ages in a vision-independent manner. Recent studies at the retinogeniculate synapse, however, have demonstrated an influence of vision on the formation of synaptic circuits in the thalamus. In mice, dark rearing from birth does not alter normal developmental maturation of the connection between retina and thalamus. However, deprivation 20 d after birth [postnatal day 20 (p20)] resulted in dramatic weakening of synaptic strength and an increase in the number of retinal inputs that innervate a thalamic relay neuron. Here, by quantifying changes in synaptic strength and connectivity in response to different time windows of deprivation, we find that several days of vision after eye opening is necessary for triggering experience-dependent plasticity. Shorter periods of visual experience do not permit similar experience-dependent synaptic reorganization. Furthermore, changes in connectivity are rapidly reversible simply by restoring normal vision. However, similar plasticity did not occur when shifting the onset of deprivation to p25. Although synapses still weakened, recruitment of additional retinal inputs no longer occurred. Therefore, synaptic circuits in the visual thalamus are unexpectedly malleable during a late developmental period, after the time when normal synapse elimination and pruning has occurred. This thalamic sensitive period overlaps temporally with experience-dependent changes in the cortex, suggesting that subcortical plasticity may influence cortical responses to sensory experience.

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Section: Discussionsupporting

confidence: 88%

Vision Triggers an Experience-Dependent Sensitive Period at the Retinogeniculate Synapse

Hooks

Chen²

2008

J. Neurosci.

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“…However, the classical view that, for example, ocular dominance plasticity arises precisely from competition-based Hebbian learning rules has come under challenge in recent years during which research has demonstrated that other activity-dependent factors are essential for both plasticity and connectional stability (Tropea et al 2009). For example, many molecular factors (Prasad et al 2002;Leamey et al 2009) including neurotrophins such as brain-derived neurotrophic factor, which promotes the formation, maturation and stabilization of inhibitory synapses, have been associated with the development of V1 in rodents and involved in regulating the critical period for experience-induced plasticity (Huang et al 1999;Fagiolini & Hensch, 2000).…”

Section: Experience-dependent Developmental Plasticitymentioning

confidence: 99%

Unravelling the development of the visual cortex: implications for plasticity and repair

Bourne

2010

Journal of Anatomy

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The visual cortex comprises over 50 areas in the human, each with a specified role and distinct physiology, connectivity and cellular morphology. How these individual areas emerge during development still remains something of a mystery and, although much attention has been paid to the initial stages of the development of the visual cortex, especially its lamination, very little is known about the mechanisms responsible for the arealization and functional organization of this region of the brain. In recent years we have started to discover that it is the interplay of intrinsic (molecular) and extrinsic (afferent connections) cues that are responsible for the maturation of individual areas, and that there is a spatiotemporal sequence in the maturation of the primary visual cortex (striate cortex, V1) and the multiple extrastriate ⁄ association areas. Studies in both humans and non-human primates have started to highlight the specific neural underpinnings responsible for the maturation of the visual cortex, and how experience-dependent plasticity and perturbations to the visual system can impact upon its normal development. Furthermore, damage to specific nuclei of the visual cortex, such as the primary visual cortex (V1), is a common occurrence as a result of a stroke, neurotrauma, disease or hypoxia in both neonates and adults alike. However, the consequences of a focal injury differ between the immature and adult brain, with the immature brain demonstrating a higher level of functional resilience. With better techniques for examining specific molecular and connectional changes, we are now starting to uncover the mechanisms responsible for the increased neural plasticity that leads to significant recovery following injury during this early phase of life. Further advances in our understanding of postnatal development ⁄ maturation and plasticity observed during early life could offer new strategies to improve outcomes by recapitulating aspects of the developmental program in the adult brain.

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“…Recent cDNA array analysis has shown that several clusters of genes may be involved in visual cortical plasticity (Prasad et al, 2002). Some specific molecules include NMDA receptors (Bear et al, 1990;Rauschecker et al, 1990;Roberts et al, 1998), neurotrophins (Maffei et al, 1992;Galuske et al, 2000;Gillespie et al, 2000), and protein kinase A (Beaver et al, 2001).…”

Section: Abstract: Creb; Ocular Dominance Plasticity; Recovery Of Fumentioning

confidence: 99%

Different Mechanisms for Loss and Recovery of Binocularity in the Visual Cortex

et al. 2002

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Diverse molecular mechanisms have been discovered that mediate the loss of responses to the deprived eye during monocular deprivation. cAMP/Ca 2ϩ response element-binding protein (CREB) function, in particular, is thought to be essential for ocular dominance plasticity during monocular deprivation. In contrast, we have very little information concerning the molecular mechanisms of recovery from the effects of monocular deprivation, even though this information is highly relevant for understanding cortical plasticity. To test the involvement of CREB activation in recovery of responses to the deprived eye, we used herpes simplex virus (HSV) to express in the primary visual cortex a dominant-negative form of CREB (HSV-mCREB) containing a single point mutation that prevents its activation. This mutant was used to suppress CREB function intracortically during the period when normal vision was restored in two protocols for recovery from monocular deprivation: reverse deprivation and binocular vision. In the reverse deprivation model, inhibition of CREB function prevented loss of responses to the newly deprived eye but did not prevent simultaneous recovery of responses to the previously deprived eye. Full recovery of cortical binocularity after restoration of binocular vision was similarly unaffected by HSV-mCREB treatment. The HSV-mCREB injections produced strong suppression of CREB function in the visual cortex, as ascertained by both DNA binding assays and immunoblot analysis showing a decrease in the expression of the transcription factor C/EBP␤, which is regulated by CREB. These results show a mechanistic dichotomy between loss and recovery of neural function in visual cortex; CREB function is essential for loss but not for recovery of deprived eye responses.

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Gene expression patterns during enhanced periods of visual cortex plasticity

Cited by 37 publications

References 34 publications

Vision Triggers an Experience-Dependent Sensitive Period at the Retinogeniculate Synapse

Vision Triggers an Experience-Dependent Sensitive Period at the Retinogeniculate Synapse

Unravelling the development of the visual cortex: implications for plasticity and repair

Different Mechanisms for Loss and Recovery of Binocularity in the Visual Cortex

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