TrpV1 receptor activation rescues cognition-relevant network dynamics in mouse hippocampus in an acute Alzheimer disease model providing a novel therapeutic target.
Neural oscillations are a necessary consequence of efficient coding of sensory signals by a spiking neural network, limited by synaptic delays and noise.
Using a sequential neurofeedback-arm reaching task, a new link is established among population neural activity patterns, generation of beta oscillations, and motor behavior changes.
Hippocampal area CA2 controls low gamma and ripple oscillations, brain waves known to be impaired in schizophrenia, implicating this important brain region in cognition.
Computational modelling shows that coupled theta and gamma oscillations in the auditory cortex can decompose speech into its syllabic constituents, and organize the neural spiking at faster timescale into a decodable format.
Random fluctuations in neuronal firing may enable a single brain region, the medial entorhinal cortex, to perform distinct roles in cognition (by generating gamma waves) and spatial navigation (by producing a grid cell map).
Stochasticity introduced computationally into a gene expression oscillator creates heterogeneity in the time of differentiation of identical cells and offers robustness to the progenitor state and the outcome of cell division.
Phase-locking of hippocampal theta and gamma waves has been proposed to support memory formation, but an analysis using robust statistical methods finds no convincing evidence for the phenomenon.
