760 research outputs found

    Animals Models of Amblyopia, in Amblyopia: challenges and opportunities

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    Visual perception: An alternative view of perceptual rivalry

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    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

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    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

    Enhancement of visual cortex plasticity by dark exposure

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    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

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    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

    Die S19 mRNS-Expression in Plattenepithelkarzinomen des oberen Aerodigestivtraktes

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    Ziel dieser Arbeit war die Analyse von Ausmaß, Häufigkeit und Charakter der mRNS-Expression des ribosomalen Proteins S19 (S19) in Head and Neck Squamous Cell Carcinoma (HNSCC). Als Methode wurde die Reverse Transkription-Polymerase Chain Reaction mit spezifischen S19 Primern gewählt. Untersucht wurden 18 HNSCC Zelllinien im Vergleich mit 17 benignen Keratinozytenzelllinien sowie 30 HNSCC Gewebeproben im Vergleich mit 8 Referenz-Gewebeproben. Für den Vergleich der HNSCC Zelllinien mit den benignen Keratinozytenzelllinien konnten die DDRT-PCR Voruntersuchungen bestätigt werden: In den HNSCC Zelllinien fand sich eine signifikante S19 mRNS-Repression. Niedrige S19 mRNS-Level korrelierten mit einem stärker entdifferenzierten Zellbild. Für die Gewebe zeichnete sich eine ähnliche Tendenz ab - signifikante Ergebnisse konnten jedoch nicht ermittelt werden. Lediglich eine große Karzinomausbreitung korrelierte signifikant mit niedrigen S19 mRNS-Leveln, wodurch die für die Zelllinien gewonnenen Ergebnisse gestützt werden. Um zu prüfen, ob die S19 mRNS-Repression lediglich auf veränderte Ribosomenzahlen zurückzuführen war, wurden zwei weiterer ribosomale Proteine, S6 und S14, mit derselben Methodik untersucht. Die mRNS-Expressionslevel aller drei ribosomalen Proteine zeigten hohe Korrelationen. Dies spricht für einen Zusammenhang der ribosomalen Rolle des S19 mit seiner mRNS-Repression in HNSCC. Die Ursachen der S19 mRNS-Repression in HNSCC wurden im Rahmen dieser Arbeit nicht näher untersucht. Ungeklärt bleibt die Frage, ob die S19 mRNS-Repression Ursache oder Folge der malignen Degeneration ist und ob ribosomale oder extraribosomale Funktionen des S19 betroffen sind. Weitere Untersuchungen sind nötig, um einen möglichen Einsatz des S19 als Tumormarker und Verlaufsparameter oder aber Zielprotein für therapeutische Interventionen abzuklären
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