Cortical plasticity: learning while you sleep?
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Sleep has been suggested to facilitate memory consolidation or learning, but there has been little direct evidence of a link between synaptic plasticity and sleep. A recent study suggests a role for sleep in the plastic changes that the visual cortex undergoes in response to occlusion of one eye early in life. (+info)
Vision research: losing sight of eye dominance.
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Most people prefer to use their right eye for viewing. New evidence reveals that this dominance is much more plastic than that for one hand or foot: it changes from one eye to the other depending on angle of gaze. Remarkably, sighting dominance depends on the hand being directed towards the visual target. (+info)
Experience-dependent plasticity of mouse visual cortex in the absence of the neuronal activity-dependent marker egr1/zif268.
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Neuronal activity elicits a rapid increase in the expression of several immediate early genes (IEGs). To clarify a role for IEG response in activity-dependent development, we examined the contribution of the egr1/zif268 gene during visual cortical processing and plasticity in mice. We first analyzed the expression of egr1 mRNA in wild-type (WT) mice using Northern blot hybridization. In the visual cortex, expression of egr1 mRNA increased dramatically after eye opening, systemic injection of kainate, or 30 min of photostimulation after a brief (5 d) period of dark adaptation. Thus, the expression of egr1 is regulated by synaptic activity in the mouse visual cortex, as it is in other species (e.g., monkeys, cats, and rats). To evaluate whether this transcription factor is directly involved in activity-dependent plasticity, mice lacking Egr1 were deprived of the use of one eye during the developmental critical period [postnatal day 24 (P24)-P34]. Extracellular in vivo single-unit recordings from the binocular zone of the visual cortex revealed that visual responses developed normally in egr1 knock-out (KO) mice. Moreover, a similarly significant shift of responsiveness in favor of the open eye was produced in both KO and WT mice by either brief (4 d) or long-term (>2 weeks) occlusion of one eye. There was no apparent compensation among egr2, egr3, or c-fos mRNA and protein expression in the visual cortex of egr1 KO mice. Taken together, these results indicate that egr1 is a useful marker of sensory input in mice but is not intrinsically necessary for the experience-dependent plasticity of the visual cortex. Our findings underscore a mechanistic distinction between sensory plasticity and long-lasting forms of synaptic potentiation in the hippocampus, for which egr1/zif268 was recently found to be essential. (+info)
cAMP/Ca2+ response element-binding protein function is essential for ocular dominance plasticity.
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The monocular deprivation model of amblyopia is characterized by a reduction in cortical responses to stimulation of the deprived eye. Although the effects of monocular deprivation on the primary visual cortex have been well characterized physiologically and anatomically, the molecular mechanisms underlying ocular dominance plasticity remain unknown. Previous studies have indicated that the transcription factor adenosine cAMP/Ca(2+) response element-binding protein (CREB) is activated during monocular deprivation. However, it remains unknown whether CREB function is required for the loss of cortical responses to the deprived eye. To address this issue, we used the herpes simplex virus (HSV) to express a dominant negative form of CREB (HSV-mCREB) containing a single point mutation that prevents its activation. Quantitative single-unit electrophysiology showed that cortical expression of this mutated form of CREB during monocular deprivation prevented the loss of responses to the deprived eye. This effect was specific and not related to viral toxicity, because overexpression of functional CREB or expression of beta-galactosidase using HSV injections did not prevent the ocular dominance shift during monocular deprivation. Additional evidence for specificity was provided by the finding that blockade of ocular dominance plasticity was reversible; animals treated with HSV-mCREB recovered ocular dominance plasticity when mCREB expression declined. Moreover, this effect did not result from a suppression of sensory responses caused by the viral infection because neurons in infected cortex responded normally to visual stimulation. These findings demonstrate that CREB function is essential for ocular dominance plasticity. (+info)
Oscillatory neuronal synchronization in primary visual cortex as a correlate of stimulus selection.
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Spike and local field potential activity were recorded simultaneously from multiple sites in primary visual cortex of strabismic cats, while monocular stimulation alternated with dichoptic stimulation, inducing interocular rivalry. During interocular rivalry, there is competition between the two nonfusible stimuli presented to the two eyes, and only one stimulus is selected at any time. We biased this competition in three different ways: (1) we exploited the condition that in strabismic cats there is often one dominant eye that is selected for most of the time. (2) We presented the two stimuli with a temporal offset, which biases competition in favor of the newly appearing stimulus. (3) We presented the two stimuli with highly different contrasts, which biases competition in favor of the stimulus with higher contrast. Whenever competition was biased in favor of the stimulus activating the recorded neurons, gamma-frequency synchronization of the respective responses was enhanced, and vice versa. Firing rates showed some differences between stimulation conditions. However, when present, these changes were inversely related to a competitive advantage of the respective stimulus. We hypothesize that enhanced gamma-frequency synchronization in primary visual cortex is a correlate of stimulus selection. Synchronization is likely to be translated into firing rate changes at later processing stages. (+info)
Protein synthesis in the visual cortex is needed for ocular dominance plasticity.
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Experience-dependent remodelling of neural connections progresses through stages, and early phases eventually give way to later long-lasting ones. The transition from early to late stages, often associated with structural changes, depends on protein synthesis. Suppression of cortical but not geniculate protein synthesis blocks ocular dominance plasticity at its earliest stage, suggesting that structural changes occur rapidly in the visual cortex following monocular deprivation. (+info)
Rapid ocular dominance plasticity requires cortical but not geniculate protein synthesis.
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Synaptic plasticity is a multistep process in which rapid, early phases eventually give way to slower, more enduring stages. Diverse forms of synaptic change share a common requirement for protein synthesis in the late stages of plasticity, which are often associated with structural rearrangements. Ocular dominance plasticity in the primary visual cortex (V1) is a long-lasting form of activity-dependent plasticity comprised of well-defined physiological and anatomical stages. The molecular events underlying these stages remain poorly understood. Using the protein synthesis inhibitor cycloheximide, we investigated a role for protein synthesis in ocular dominance plasticity. Suppression of cortical, but not geniculate, protein synthesis impaired rapid ocular dominance plasticity, while leaving neuronal responsiveness intact. These findings suggest that structural changes underlying ocular dominance plasticity occur rapidly following monocular occlusion, and cortical changes guide subsequent alterations in thalamocortical afferents. (+info)
Correlation model for joint development of refined retinotopic map and ocular dominance columns.
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We describe a modification to a standard correlation model for the development of the geniculocortical projection that relays visual input to the visual cortex. The modification is to include threshold-activation of cortical cells as opposed to linear activation and it is shown that this can account for topographic map refinement (TMR). This contrasts with other models that require cortical cells to compete for activation or for neurotrophic support. Simulations are conducted for the joint development of ocular dominance columns and TMR in normal animals and parameter variations are used to both confirm robustness and to simulate some experimental conditions. (+info)