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Pet1 neurons actively maintain cardiorespiratory tone and dynamic range in mouse neonates and critically support the recovery response to apneas, informing brain findings in the sudden infant death syndrome.

V1 damage impairs unconscious following movements of stimulus motion, even after conscious perception has been restored through psychophysical training, thus demonstrating distinct neural pathways for perception and action.

After complete spinal transection in adult rats, careful combinations of pharmacological and physical therapies create a novel cortical sensorimotor circuit that may bypass the lesion through biomechanical coupling, allowing animals to recover unassisted hindlimb locomotion.

A genetically-defined population of spinal interneurons is reciprocally connected with spinal locomotor circuits and mediates recovery of locomotor function following spinal cord transection.

Persistence of severe acute respiratory syndrome coronavirus 2 and reactivation of unrelated latent viruses may play a role in the development and pathogenesis of long COVID, and future research should focus on identifying the mechanisms behind these interactions.

Sequential introduction of transcription factors enables large-scale generation of induced motor neurons (iMNs) from human somatic cells, and transplantation of iMNs exhibit therapeutic effects in spinal cord injury model.

Precisely-timed bursts of closed-loop vagus nerve stimulation during rehabilitation restore neural connectivity and substantially improve recovery of motor function after SCI.

Mice that viewed a visual stimulus whilst running showed recovery of the neuronal responses that had been lost due to early visual deprivation, with potential relevance for amblyopia.

Photobleaching and recovery of a fluorescent glutamate sensor enable demonstration of the distinct spatial architectures of spontaneous versus evoked forms of glutamatergic neurotransmission within single synapses.

The initiation of DNA damage checkpoint recovery involves ATM-mediated E3 ubiquitin ligase E6AP phosphorylation which disrupts E6AP-MASTL association and leads to MASTL protein accumulation and cell cycle resumption.