Operant drug self-administration in a mouse model of neuropathic pain reveals pain-relieving effects of a cannabinoid CB2 receptor agonist that are mediated through CB2 receptors of neurons and lymphocytes.
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.
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.
Dysfunctions of myelin peroxisomes cause a lysosomal storage-like disorder associated with alterations in glial and axonal membranes, which is the likely cause of nerve impairment in peroxisomal disorders.
The flow of somatosensory information through the spinal dorsal horn is regulated by synaptic inhibition, which acts upon excitatory and inhibitory interneurons, but the former are especially prone to disinhibition.