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References in periodicals archive ?
Drager, "Observations on monocular deprivation in mice," Journal of Neurophysiology, vol.
Bear, "Molecular mechanism for loss of visual cortical responsiveness following brief monocular deprivation," Nature Neuroscience, vol.
Lunghi, "Short-term monocular deprivation enhances physiological pupillary oscillations," Neural Plasticity, vol.
The other approach [12, 22, 24] has involved the use of fusible stimuli by measuring the contribution that each eye makes to the binocularly fused percept and how this eye balance is perturbed by short-term monocular deprivation. Here we use this latter approach to assess what contribution physical activity makes to the neuroplastic modulation of ocular dominance.
Morrone, "Brief periods of monocular deprivation disrupt ocular balance in human adult visual cortex," Current Biology, vol.
Morrone, "Long-term effects of monocular deprivation revealed with binocular rivalry gratings modulated in luminance and in color," Journal of Vision, vol.
A recent study has shown that following 2.5 hours of monocular deprivation GABA concentration (measured by means of Magnetic Resonance Spectroscopy at 7-Tesla) drops in the adult primary visual cortex and across subjects the decrease in GABA levels highly correlates with the boost of deprived eye during binocular rivalry [4].
We measured binocular rivalry and pupil diameter before and after 2 hours of monocular deprivation. The measurements obtained before the deprivation were used as baseline (two 180 sec experimental blocks for binocular rivalry, one 120 sec block of pupillary measurement).
Previous studies have shown that 7 days period of monocular deprivation in fluoxetine-treated adult rats is sufficient to bring about a change in the ocular dominance.
We observed that fluoxetine produced a significant increase in the expression of genes involved in inhibitory neurotransmission when comparing both animals with binocular vision and animals with monocular deprivation with their respective controls (BV-Sal versus BV-Flx and MD-Sal versus MD-Flx; Figure 2(a)).
Indeed, transgenic mice with reduced levels of intracortical inhibition due to the lack of the GABA-synthetizing enzyme GAD65 exhibit no modifications of visual cortex responsiveness after monocular deprivation in early life, whereas enhancing inhibition by exogenous administration of GABAA-receptor agonists in the knockout background rescues the impairment of plasticity [86, 87].
Compelling experimental evidence for NPAS4-mediated transcriptional mechanisms that lie behind phenomena of visual cortex plasticity in adulthood has been recently obtained using the monocular deprivation paradigm and chronic treatment with fluoxetine as a pharmacological strategy for the induction of plasticity.