Visual perception: An alternative view of perceptual rivalry

AbstractThe mechanism by which one or the other view of an ambiguous figure — such as the Necker cube — gains dominance has been unclear. Recent evidence suggests that the right frontoparietal cortex is responsible for the selection process, and that each cortical hemisphere represents one of the two rivalling percepts

Visual perception: Spotlight on the primary visual cortex

AbstractVisual search tasks appear to involve spatially selective attention to the target, but evidence for attentional modulation in the visual area with the most precise retinotopic organization – V1 – has been elusive. Recent imaging studies show that spatial attention can indeed enhance visual responses in human V1

Plasticity of the visual cortex and treatment of amblyopia [Review]

Over the last 50 years, research into the developmental plasticity of the visual cortex has led to a growing understanding of first the causes and then of the underlying cellular mechanisms of amblyopia or ‘lazy eye’, the commonest childhood disorder of vision. While it is widely believed that amblyopia cannot be treated successfully after the age of about 7, recent animal studies have demonstrated that visual cortex plasticity can be restored or enhanced later in life, paving the way for new strategies for the treatment of amblyopia that attempt to remove molecular brakes on plasticity. In addition, both animal and human work has established that amblyopia is not simply a monocular deficit, and therefore the most promising new non-invasive approaches force the two eyes to cooperate as opposed to conventional procedures that severely penalise the good eye

Enhancement of visual cortex plasticity by dark exposure

Dark rearing is known to delay the time course of the critical period for ocular dominance plasticity in the visual cortex. Recent evidence suggests that a period of dark exposure (DE) may enhance or reinstate plasticity even after closure of the critical period, mediated through modification of the excitatory–inhibitory balance and/or removal of structural brakes on plasticity. Here, we investigated the effects of a week of DE on the recovery from a month of monocular deprivation (MD) in the primary visual cortex (V1) of juvenile mice. Optical imaging of intrinsic signals revealed that ocular dominance in V1 of mice that had received DE recovered slightly more quickly than of mice that had not, but the level of recovery after three weeks was similar in both groups. Two-photon calcium imaging showed no significant difference in the recovery of orientation selectivity of excitatory neurons between the two groups. Parvalbumin-positive (PV+) interneurons exhibited a smaller ocular dominance shift during MD but again no differences in subsequent recovery. The percentage of PV+ cells surrounded by perineuronal nets, a structural brake on plasticity, was lower in mice with than those without DE. Overall, DE causes a modest enhancement of mouse visual cortex plasticity

Spatial memory engram in the mouse retrosplenial cortex

Memory relies on lasting adaptations of neuronal properties elicited by stimulus-driven plastic changes [1]. The strengthening (and weakening) of synapses results in the establishment of functional ensembles. It is presumed that such ensembles (or engrams) are activated during memory acquisition and re-activated upon memory retrieval. The retrosplenial cortex (RSC) has emerged as a key brain area supporting memory [2], including episodic and topographical memory in humans [3, 4, 5], as well as spatial memory in rodents [6, 7]. Dysgranular RSC is densely connected with dorsal stream visual areas [8] and contains place-like and head-direction cells, making it a prime candidate for integrating navigational information [9]. While previous reports [6, 10] describe the recruitment of RSC ensembles during navigational tasks, such ensembles have never been tracked long enough to provide evidence of stable engrams and have not been related to the retention of long-term memory. Here, we used in vivo 2-photon imaging to analyze patterns of activity of over 6,000 neurons within dysgranular RSC. Eight mice were trained on a spatial memory task. Learning was accompanied by the gradual emergence of a context-specific pattern of neuronal activity over a 3-week period, which was re-instated upon retrieval more than 3 weeks later. The stability of this memory engram was predictive of the degree of forgetting; more stable engrams were associated with better performance. This provides direct evidence for the interdependence of spatial memory consolidation and RSC engram formation. Our results demonstrate the participation of RSC in spatial memory storage at the level of neuronal ensembles

Opa1 deficiency leads to diminished mitochondrial bioenergetics with compensatory increased mitochondrial motility

Purpose: Retinal ganglion cells (RGCs) are susceptible to mitochondrial deficits and also the major cell type affected in patients with mutations in the OPA1 gene in autosomal dominant optic atrophy (ADOA). Here, we characterized mitochondria in RGCs in vitro from a heterozygous B6; C3-Opa1Q285STOP (Opa1+/−) mouse model to investigate mitochondrial changes underlying the pathology in ADOA. Methods: Mouse RGCs were purified from wild-type and Opa1+/− mouse retina by two-step immunopanning. The mitochondria in neurites of RGCs were labeled with MitoTracker Red for structure and motility measurement by time-lapse imaging. Mitochondrial bioenergetics were determined by the real-time measurement of oxygen consumption rate using a Seahorse XFe 96 Extracellular Flux Analyzer. Results: We observed a significant decrease in mitochondrial length in Opa1+/− RGCs with a remarkably higher proportion and density of motile mitochondria along the neurites. We also observed an increased transport velocity with a higher number of contacts between mitochondria in Opa1+/− RGC neurites. The oxygen consumption assays showed a severe impairment in basal respiration, Adenosine triphosphate-linked (ATP-linked) oxygen consumption, as well as reserve respiratory capacity, in RGCs from Opa1+/− mouse retina. Conclusions: Opa1 deficiency leads to significant fragmentation of mitochondrial morphology, activation of mitochondrial motility and impaired respiratory function in RGCs from the B6; C3-Opa1Q285STOP mouse model. This highlights the significant alterations in the intricate interplay between mitochondrial morphology, motility, and energy production in RGCs with Opa1 deficiency long before the onset of clinical symptoms of the pathology

Animal models of amblyopia

AbstractUnquestionably, the last six decades of research on various animal models have advanced our understanding of the mechanisms that underlie the many complex characteristics of amblyopia as well as provided promising new avenues for treatment. While animal models in general have served an important purpose, there nonetheless remain questions regarding the efficacy of particular models considering the differences across animal species, especially when the goal is to provide the foundations for human interventions. Our discussion of these issues culminated in three recommendations for future research to provide cohesion across animals models as well as a fourth recommendation for acceptance of a protocol for the minimum number of steps necessary for the translation of results obtained on particular animal models to human clinical trials. The three recommendations for future research arose from discussions of various issues including the specific results obtained from the use of different animal models, the degree of similarity to the human visual system, the ability to generate animal models of the different types of human amblyopia as well as the difficulty of scaling developmental timelines between different species.</jats:p