C. elegans exhibits two distinct behavioural macro-states, active and quiet wakefulness, and protein kinase A regulates switching between these two states.

Dynamic calcium activity in the hippocampus changes markedly across behavioral and physiological states and depends on muscarinic acetylcholine receptor activation.

During quiet wakefulness but not slow wave sleep, reward modulated VTA neurons coordinate selectively with hippocampal replay sequences and are biased in their timing towards the reactivated representation of reward locations.

Demyelination disrupts fast inhibition of pyramidal neurons, thereby changing neocortical rhythms and causing the emergence of brief epileptic-like discharges.

Sleep and wake states are not sufficient to drive changes in neocortical synaptic strengths.

Neuropathic pain preserves mouse sleep in architecture and characteristic spectral bands but perturbs arousability in ways reminiscent of insomnia disorders, in which hyperarousal and hyperalertness to environmental stimuli are prevalent.

Activating deeper layers of the cortex using cortical electrical stimulation triggers the activation of thalamic nuclei through trans-synaptic signaling, which can result in a range of complex responses that can be detected using EEG signals.

The first patch-clamp recordings from single cerebellar granule cells during locomotion reveal that the entire step sequence can be predicted from both excitatory synaptic input and output spikes from a single neuron.

Different methods for inducing sleep in Drosophila flies may be promoting distinct sleep stages with different functions when brain activity and gene expression are compared.

The majority of hippocampal neurons in CA3 experience inhibition before and during ripple buildup, while dentate and CA1 cells display depolarizing transients preceding and following ripple onset pointing to a long and orchestrated awake ripple initiation process.