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.
Although primary sensory neuron-derived calcitonin gene-related peptide (CGRP) contributes to the processing of pain messages, an understudied population of dorsal horn CGRP-expressing interneurons also contributes to the processing of mechanical sensitivity.
Ultrastructural, biochemical, and behavioral assessments reveal that the Crtap-/- mouse model of severe, recessive Osteogenesis Imperfecta presents with defects in tendon structure and strength that correlate with severe motor deficits.
In models of chronic migraine, neuronal complexity is diminished in head-pain processing regions but restored through HDAC6 inhibition, which increases tubulin acetylation and cytoskeletal flexibility, and CGRP receptor blockade.
Alterations to brain network communication leading to a progressive loss in descending inhibitory modulation of the spinal cord is a key determinate of pain state development following peripheral nerve injury.
An interdisciplinary approach uncovers a new antinociceptive molecular mechanism and shows that the adhesion GPCR CIRL adjusts the sensation of gentle touch and noxious mechanical insult in opposite directions.