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The model, comprising both the cerebellar cortex and vestibular nuclei, reproduces behavioral data and accounts for the changes in neural activity during learning in wild type mice.
Here we resolve the cerebellar consolidation question using simultaneous, post-training inactivations of both the cerebellar cortex and nuclei.
Essential for the study was that the relevant eyeblink control regions of both the cerebellar cortex and the cerebellar nuclei were fully inactivated in the critical experimental group.
It is noticeable that the motor command (u) reaches both the predictor and this summing element, similar to the messages conveyed by the excitatory mossy fibers that reach both the cerebellar cortex and the cerebellar nuclei.
The same feedback signals reach the predictor and summing element, as the messages conveyed by the mossy fibers reach both the cerebellar cortex and cerebellar nuclei.
Many authors suggest that during delay eyeblink conditioning, plasticity occurs in both the cerebellar cortex and deep cerebellar nuclei (for reviews, see Attwell et al. 2002; Christian & Thompson 2003; De Zeeuw & Yeo 2005; Ito 2002).
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We have shown that the cerebellum is critical for motor learning, and we have provided evidence that learning occurs both in the cerebellar cortex and the deep cerebellar nuclei.
In addition, consistent apoptotic cell death was present in both layers of the cerebellar cortex in three month-old animals (Figure 4M), whereas it is significantly reduced in the four month-old rabbits, particularly in the granule cell layer (Figure 4M; summarized in Figure 4N).
Modification of gain in the vestibulo-ocular reflex (VOR) involves plasticity both in the cerebellar cortex and in Purkinje cell target neurons in the brainstem vestibular complex [1] [5] and may be representative of other forms of cerebellum-dependent motor learning [6].
Indeed, by taking into account the functional and the anatomical features of the cerebellar pathways, our model provides a coherent theoretical framework that implements the coexistence of these two internal models replicating both the functional role of the cerebellar cortex and its corresponding anatomical structure.
We speculate that the modulation of both PCs and INs endow the cerebellar cortex with the versatility to learn almost any temporal output pattern (e.g., we have modified our model to reproduce oculopalatal tremor, a clinical eye movement disorder [30]).
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