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Epilepsy can have many different causes and its development (epileptogenesis) involves a bewildering complexity of interacting processes. Here, we present a first-of-its-kind computational model to better understand the role of neuroimmune interactions in the development of acquired epilepsy. Our model describes the interactions between neuroinflammation, blood-brain barrier disruption, neuronal loss, circuit remodeling, and seizures. Formulated as a system of nonlinear differential equations, the model is validated using data from animal models that mimic human epileptogenesis caused by infection, status epilepticus, and blood-brain barrier disruption. The mathematical model successfully explains characteristic features of epileptogenesis such as its paradoxically long timescales (up to decades) despite short and transient injuries, or its dependence on the intensity of an injury. Furthermore, stochasticity in the model captures the variability of epileptogenesis outcomes in individuals exposed to identical injury. Notably, in line with the concept of degeneracy, our simulations reveal multiple routes towards epileptogenesis with neuronal loss as a sufficient but non-necessary component. We show that our framework allows for in silico predictions of therapeutic strategies, providing information on injury-specific therapeutic targets and optimal time windows for intervention.
Treatments for amblyopia focus on vision therapy and patching of one eye. Predicting the success of these methods remains difficult, however. Recent research has used binocular rivalry to monitor visual cortical plasticity during occlusion therapy, leading to a successful prediction of the recovery rate of the amblyopic eye. The underlying mechanisms and their relation to neural homeostatic plasticity are not known. Here we propose a spiking neural network to explain the effect of short-term monocular deprivation on binocular rivalry. The model reproduces perceptual switches as observed experimentally. When one eye is occluded, inhibitory plasticity changes the balance between the eyes and leads to longer dominance periods for the eye that has been deprived. The model suggests that homeostatic inhibitory plasticity is a critical component of the observed effects and might play an important role in the recovery from amblyopia.
The development of binocular vision is an active learning process comprising the development of disparity tuned neurons in visual cortex and the establishment of precise vergence control of the eyes. We present a computational model for the learning and self-calibration of active binocular vision based on the Active Efficient Coding framework, an extension of classic efficient coding ideas to active perception. Under normal rearing conditions with naturalistic input, the model develops disparity tuned neurons and precise vergence control, allowing it to correctly interpret random dot stereograms. Under altered rearing conditions modeled after neurophysiological experiments, the model qualitatively reproduces key experimental findings on changes in binocularity and disparity tuning. Furthermore, the model makes testable predictions regarding how altered rearing conditions impede the learning of precise vergence control. Finally, the model predicts a surprising new effect that impaired vergence control affects the statistics of orientation tuning in visual cortical neurons.
A key competence for open-ended learning is the formation of increasingly abstract representations useful for driving complex behavior. Abstract representations ignore specific details and facilitate generalization. Here we consider the learning of abstract representations in a multi-modal setting with two or more input modalities. We treat the problem as a lossy compression problem and show that generic lossy compression of multimodal sensory input naturally extracts abstract representations that tend to strip away modalitiy specific details and preferentially retain information that is shared across the different modalities. Furthermore, we propose an architecture to learn abstract representations by identifying and retaining only the information that is shared across multiple modalities while discarding any modality specific information.