Altered brain state during episodic dystonia in tottering mice decouples primary motor cortex from limb kinematics.

Episodic Ataxia Type 2 (EA2) is a rare neurological disorder caused by a mutation in the gene, encoding the P/Q-type voltage-gated Ca channel important for neurotransmitter release. Patients with this channelopathy exhibit both cerebellar and cerebral pathologies, suggesting the condition affects both regions. The mouse is the most commonly used EA2 model due to an orthologous mutation in the gene.

Relative salience signaling within a thalamo-orbitofrontal circuit governs learning rate.

Learning to predict rewards is essential for the sustained fitness of animals. Contemporary views suggest that such learning is driven by a reward prediction error (RPE)-the difference between received and predicted rewards. The magnitude of learning induced by an RPE is proportional to the product of the RPE and a learning rate.

Cortex-wide neural interfacing via transparent polymer skulls.

Neural computations occurring simultaneously in multiple cerebral cortical regions are critical for mediating behaviors. Progress has been made in understanding how neural activity in specific cortical regions contributes to behavior. However, there is a lack of tools that allow simultaneous monitoring and perturbing neural activity from multiple cortical regions.