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Enhanced visual experience rehabilitates the injured brain in Xenopus tadpoles in an NMDAR-dependent manner.

Traumatic brain injuries introduce functional and structural circuit deficits that must be repaired for an organism to regain function. We developed an injury model in which Xenopus laevis tadpoles are given a penetrating stab wound that damages the optic tectal circuit and impairs visuomotor behavior. In tadpoles, as in other systems, injury induces neurogenesis. The newly generated neurons are thought to integrate into the existing circuit, however, whether they integrate via the same mechanisms that govern normal neuronal maturation during development is not understood. Development of the functional visuomotor circuit in Xenopus is driven by sensory activity. We hypothesized that enhanced visual experience would improve recovery from injury and by facilitating integration of newly generated neurons into the tectal circuit. We labeled newly generated neurons in the injured tectum by GFP expression and examined their circuit integration using electrophysiology and in vivo imaging. Providing animals with brief bouts of enhanced visual experience starting 24 hours after injury increased synaptogenesis and circuit integration of new neurons, and facilitated behavioral recovery. To investigate mechanisms of neuronal integration and behavioral recovery after injury, we interfered with NMDA receptor function. Ifenprodil, which blocks GluN2B-containing NMDA receptors, impaired dendritic arbor elaboration. GluN2B blockade inhibited functional integration of neurons generated in response to injury and prevented behavioral recovery. Furthermore, tectal GluN2B knockdown blocked the beneficial effects of enhanced visual experience on functional plasticity and behavioral recovery. We conclude that visual experience-mediated rehabilitation of the injured tectal circuit occurs by GluN2B-containing NMDAR-dependent integration of newly generated neurons.

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