Disease relevance of Dominance, Ocular

• PURPOSE: To determine the association between ocular dominance and degree of myopia in patients with anisometropia [1].
• It is unknown whether the ocular dominance columns are affected in amblyopia produced by strabismus [2].
• The effects of microiontophoretic bicuculline, a gamma-aminobutyric acid (GABA) antagonist, on the ocular dominance of visual cortical neurons were compared in normal cats and cats reared with abnormal monocular visual experience (monocular deprivation, surgical strabismus, and monocular deprivation after dark rearing) [3].

Psychiatry related information on Dominance, Ocular

• Here we show that inhibition of protein kinase A (PKA) by Rp-8-Cl-cAMPS blocks ocular dominance shifts that occur following monocular deprivation early in the critical period [4].

High impact information on Dominance, Ocular

• Hypotheses about the mechanisms underlying ocular-dominance plasticity assume the activation of NMDA (N-methyl-D-aspartate) receptors and subsequent calcium influx as a trigger of synaptic modifications [5].
• The staining for GABA and GAD in neuronal somata and terminals was markedly reduced within ocular dominance columns associated with a removed or a visually deprived eye, suggesting that the GABA concentration in cortical neurones may depend on their levels of activity [6].
• In the present study, patterns of ocular dominance and orientation selectivity were obtained repeatedly from the same patch of cortex using the dye merocyanine oxazolone, together with current image-processing techniques [7].
• These include the co-localization of glutamic acid decarboxylase (GAD, the biosynthetic enzyme of the inhibitory neurotransmitter, gamma-aminobutyric acid) with the mitochondrial enzyme, cytochrome oxidase (CO) in functionally distinct subcompartments of ocular dominance columns [8].
• Ocular dominance plasticity under metabotropic glutamate receptor blockade [9].

Biological context of Dominance, Ocular

• The maintenance of GluR2 in these output layers is governed by visual input and neuronal activity, as monocular impulse blockade induced a down-regulation of this subunit in deprived ocular dominance columns [10].
• This suggests that NOS activity is not downstream of NMDA receptor activation during retinotectal synaptic competition because NMDA receptor activation is necessary for segregation of retinal afferents into ocular dominance stripes in the doubly innervated tadpole optic tectum [11].

Anatomical context of Dominance, Ocular

• Cyclic AMP-dependent protein kinase mediates ocular dominance shifts in cat visual cortex [4].
• We then hypothesized that SCG10 family molecules, known for catastrophic factors of microtubules, play important roles in the formation of ocular dominance columns [12].
• Co-localization in layer 4 neurons overlaps the period of ocular dominance segregation, suggesting that the onset of cortical maturity coincides with segregation of calcium-binding proteins within the GABA interneurons [13].
• These results indicate that the monocular deprivation during the sensitive period of ocular dominance plasticity modified beta1-adrenergic receptor immunoreactivity, including that in glial cells [14].
• This study was designed to determine whether eye-dominance affects head posture (rotation) and in turn, whether head posture is associated with mandibular frenum midline deviation, in both TMJ and control subjects [15].

Associations of Dominance, Ocular with chemical compounds

• Using the protein synthesis inhibitor cycloheximide, we investigated a role for protein synthesis in ocular dominance plasticity [16].
• Additionally, domains sharing the ocular dominance and orientation preference of the neurons at the injection sites were visualized by 2-deoxyglucose (2-DG) autoradiography [17].
• This rearing reduced the degree of binocular interaction in striate cortical neurons and caused a modest shift in eye dominance away from the atropine-treated eye [18].
• This "binocular" spread of DG uptake into the inappropriate eye dominance strip in 4Ca may be related to the appearance of orientation tuning and orientation columns in that layer [19].
• Nevertheless, blockade of NOS with daily injections of nitroarginine from P14 to P56 fails to prevent the formation of ocular dominance columns, although NOS activity is reduced by >98% [20].

Gene context of Dominance, Ocular

• Inhibition of ocular dominance column formation by infusion of NT-4/5 or BDNF [21].
• Enhanced NR2A subunit expression and decreased NMDA receptor decay time at the onset of ocular dominance plasticity in the ferret [22].
• In particular, recent studies have shown that Trk B ligands are involved in the formation of the ocular dominance columns during postnatal development [23].
• We find that mutations in the Nogo-66 receptor (NgR) affect cessation of ocular dominance plasticity [24].
• BDNF is less effective on ocular dominance plasticity and, in addition, strongly affects spontaneous and visually evoked activity in cortical neurons [25].

Analytical, diagnostic and therapeutic context of Dominance, Ocular

• Localized microperfusion of propranolol into the kitten visual cortex reduced the expected shift in the ocular dominance approximately 2 mm away from the center of perfusion [26].
• To label retrogradely subplate neurons, fluorescent latex microspheres were injected into primary visual cortex of postnatal day 28 ferrets, just prior to the onset of ocular dominance column formation [27].
• By using immunohistochemistry techniques, we tested the hypothesis of the role of subunit R1 of NMDA (NMDAR1) receptors in the thalamocortical afferent segregation into ocular-dominance columns in the New World monkey, Callithrix jacchus [28].
• The segregation of ocular dominance patches or columns has been studied using a variety of anatomical pathway-tracing techniques, by electrophysiological recording of postsynaptic units or field potentials, and by the 2-deoxyglucose method following visual stimulation of only one eye [29].
• Substantial reduction of noradrenaline in kitten visual cortex by intraventricular injections of 6-hydroxydopamine does not always prevent ocular dominance shifts after monocular deprivation [30].

References