Changes in contrast sensitivity induced by defocus and their possible relations to emmetropization in the chicken.
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PURPOSE: To test whether the level of contrast adaptation (CA) relates to refractive development in the chicken. (CA refers to a spatial frequency-selective increase of suprathreshold contrast sensitivity after exposure to low-contrast patterns). METHODS: CA was determined in individual chicks by comparing their optomotor gain in response to drifting low-contrast stripe patterns before and after treatment with spectacle lenses. The amount of CA was compared with the loss of contrast predicted from defocus at the tested spatial frequency. The reversion of CA and recovery from deprivation myopia were studied while the retinal image features were controlled by forcing the animals to watch spatially filtered digital video clips. RESULTS: CA was induced by wearing positive and negative lenses for 1.5 hours, both without and with cycloplegia, but was less pronounced in the case of positive lenses when accommodation was intact. The amount of CA at a tested spatial frequency was predicted from the loss of contrast calculated from the modulation transfer function for a defocused optical system. Watching low-pass-filtered video clips induced deprivation myopia and inhibited recovery from it. It also prevented the reversal of CA that was previously induced by deprivation. Both recovery from deprivation myopia and recovery from CA occurred with sharp video clips, although less so than with normal visual exposure. CONCLUSIONS: CA changes with retinal image sharpness and occurs even when accommodation is intact. Because CA correlates with myopia induced by frosted occluders, negative lenses, and low-pass-filtered video clips, and its reversal correlates with recovery from myopia, it is possible that shifts in CA may represent a signal related to refractive error development. (+info)
Visual deprivation alters development of synaptic function in inner retina after eye opening.
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Visual deprivation impedes refinement of neuronal function in higher visual centers of mammals. It is often assumed that visual deprivation has minimal effect, if any, on neuronal function in retina. Here we report that dark rearing reduces the light-evoked responsiveness of inner retinal neurons in young mice. We also find that 1 to 2 weeks after eye opening, there is a surge (>4-fold) in the frequency of spontaneous excitatory and inhibitory synaptic events in ganglion cells. Dark rearing reversibly suppresses this surge, but recovery takes >6 days. Frequency changes are not accompanied by amplitude changes, indicating that synaptic reorganization is likely to be presynaptic. These findings indicate there is a degree of activity-dependent plasticity in the mammalian retina that has not been previously described. (+info)
Putative feed-forward control of jaw-closing muscle activity during rhythmic jaw movements in the anesthetized rabbit.
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When a thin plastic test strip of various hardness is placed between the upper and lower teeth during rhythmical jaw movements induced by electrical stimulation of the cortical masticatory area (CMA) in anesthetized rabbits, electromyographic (EMG) activity of the masseter muscle is facilitated in a hardness-dependent manner. This facilitatory masseteric response (FMR) often occurred prior to contact of the teeth to the strip, and thus preceded the onset of the masticatory force. Since this finding suggests involvement of a feed-forward mechanism in the induction of the FMR, the temporal relationship between the onset of the FMR and that of the masticatory force was analyzed in five sequential masticatory cycles after application of the strip. The FMR was found to precede the onset of masticatory force from the second masticatory cycle after application of the strip, but never did in the first cycle. This finding supports the concept of a feed-forward control mechanism that modulates FMR timing. Furthermore, the FMR preceding the force onset disappeared after making a lesion of the mesencephalic trigeminal nucleus (MesV) where the ganglion cells of the muscle spindle afferents from the jaw-closing muscles are located. In contrast, no such change occurred after blocking periodontal afferents by transection of both the maxillary and the inferior alveolar nerves. The putative feed-forward control of the FMR is therefore dependent mainly on sensory inputs from the muscle spindles, but little on those from the periodontal receptors, if any. We further examined the involvement of the CMA with the putative feed-forward control of the FMR via the transcortical loop. For this purpose, rhythmical jaw movements were induced by stimulation of the pyramidal tract. No significant change in the timing of the FMR occurred after the CMA ablation, which strongly suggests that the CMA is not involved in the putative feed-forward control of the FMR. The FMR was also noted to increase significantly in a hardness-dependent manner even after the MesV lesion, although the rate of increment decreased significantly. Contribution of muscle spindles and periodontal receptors to the hardness-dependent change of the FMR is discussed. (+info)
A role for the cytoplasmic polyadenylation element in NMDA receptor-regulated mRNA translation in neurons.
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The ability of neurons to modify synaptic connections based on activity is essential for information processing and storage in the brain. The induction of long-lasting changes in synaptic strength requires new protein synthesis and is often mediated by NMDA-type glutamate receptors (NMDARs). We used a dark-rearing paradigm to examine mRNA translational regulation in the visual cortex after visual experience-induced synaptic plasticity. In this model system, we demonstrate that visual experience induces the translation of mRNA encoding the alpha-subunit of calcium/calmodulin-dependent kinase II in the visual cortex. Furthermore, this increase in translation is NMDAR dependent. One potential source for newly synthesized proteins is the translational activation of dormant cytoplasmic mRNAs. To examine this possibility, we developed a culture-based assay system to study translational regulation in neurons. Cultured hippocampal neurons were transfected with constructs encoding green fluorescent protein (GFP). At 6 hr after transfection, approximately 35% of the transfected neurons (as determined by in situ hybridization) expressed detectable GFP protein. Glutamate stimulation of the cultures at this time induced an increase in the number of neurons expressing GFP protein that was NMDAR dependent. Importantly, the glutamate-induced increase was only detected when the 3'-untranslated region of the GFP constructs contained intact cytoplasmic polyadenylation elements (CPEs). Together, these findings define a molecular mechanism for activity-dependent synaptic plasticity that is mediated by the NMDA receptor and requires the CPE-dependent translation of an identified mRNA. (+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)
Better perception of global motion after monocular than after binocular deprivation.
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We used random-dot kinematograms to compare the effects of early monocular versus early binocular deprivation on the development of the perception of the direction of global motion. Patients had been visually deprived by a cataract in one or both eyes from birth or later after a history of normal visual experience. The discrimination of direction of global motion was significantly impaired after early visual deprivation. Surprisingly, impairments were significantly worse after early binocular deprivation than after early monocular deprivation, and the sensitive period was very short. The unexpectedly good results after monocular deprivation suggest that the higher centers involved in the integration of global motion profit from input to the nondeprived eye. These findings suggest that beyond the primary visual cortex, competitive interactions between the eyes can give way to collaborative interactions that enable a relative sparing of some visual functions after monocular deprivation. (+info)
Effects of brief periods of unrestricted vision on the development of form-deprivation myopia in monkeys.
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PURPOSE: To characterize the temporal integration properties of the mechanisms responsible for form-deprivation myopia (FDM), the effects of brief daily periods of unrestricted vision on the degree of FDM were investigated in infant monkeys. METHODS: Starting at approximately 3 weeks of age, unilateral form deprivation was produced in 24 infant rhesus monkeys by securing a diffuser spectacle lens in front of one eye and a clear, zero-powered lens in front of the fellow eye. During the treatment period (17 +/- 2 weeks), six infants wore the diffuser lenses continuously. In the other experimental infants, the diffuser lenses were removed each day and replaced with clear, zero-powered lenses for 1 (n = 7), 2 (n = 7), or 4 hours (n = 4). Refractive development was assessed by retinoscopy and A-scan ultrasonography. Control data were obtained from 11 normal infants and 3 infants reared with zero-powered lenses over both eyes. RESULTS: The degree of FDM varied significantly with the duration of unrestricted vision. Continuous form deprivation produced -5.2 +/- 3.6 D of relative axial myopia. However, 1 hour of unrestricted vision was sufficient to reduce the degree of axial FDM by more than 50% (-1.7 +/- 3.2 D). The infants that were allowed 4 hours of unrestricted vision exhibited only -0.4 +/- 0.5 D of FDM. CONCLUSIONS: As observed in chickens and tree shrews, relatively long periods of form deprivation can be counterbalanced by quite short periods of unrestricted vision. These results indicate that the processes or signals that promote axial elongation in monkeys are comparatively weak or easily overridden by factors that slow ocular growth. (+info)
Expression of the nerve growth factor receptors TrkA and p75NTR in the visual cortex of the rat: development and regulation by the cholinergic input.
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Several lines of evidence have shown that nerve growth factor (NGF), the progenitor of the neurotrophin family of growth factors, plays a fundamental role in the developmental plasticity of the rat visual cortex. However, the expression of NGF receptors (NGFRs) TrkA and p75(NTR) and the possible sites of NGF action in the visual cortex remain to be elucidated so far. Using a highly sensitive ECL immunoblot analysis, we have been able to show, in the present study, that the TrkA protein is expressed in the rat visual cortex and that it is developmentally upregulated during the critical period for cortical plasticity. In contrast, the expression level of the low-affinity NGF receptor p75(NTR) seems to remain nearly constant throughout development. In the analysis of possible pathways involved in the regulation of NGFR expression, we found that neither blockade of the visual input nor NGF administration to the visual cortex resulted in a modulation of NGFR levels of expression. On the other hand, the selective destruction of cholinergic afferents to the visual cortex caused a dramatic, but not complete, reduction of the cortical NGFRs, which suggests that these receptors are located on cholinergic terminals predominantly. At the functional level, we found that, after the elimination of the cholinergic afferents to the visual cortex, the NGF-induced increase of both acetylcholine and glutamate release from cortical synaptosomes was strongly impaired. These results indicate that the cholinergic input is an important mediator of visual cortex responsiveness to NGF action. (+info)