title: Plasticity of inhibition in the spinal cord.
abstract: Inhibitory interneurons, which use GABA and/or glycine as their principal transmitter, have numerous roles in regulating the transmission of sensory information through the spinal dorsal horn. These roles are likely to be performed by different populations of interneurons, each with specific locations in the synaptic circuitry of the region. Peripheral nerve injury frequently leads to neuropathic pain, and it is thought that loss of function of inhibitory interneurons in the dorsal horn contributes to this condition. Several mechanisms have been proposed for this disinhibition, including death of inhibitory interneurons, decreased transmitter release, diminished activity of these cells and reduced effectiveness of GABA and glycine as inhibitory transmitters. However, despite numerous studies on this important topic, it is still not clear which (if any) of these mechanisms contributes to neuropathic pain after nerve injury.
authors.affiliation: Institute of Neuroscience and Psychology, College of Medical Veterinary and Life Sciences, University of Glasgow, Glasgow, G12 8QQ, UK, andrew.todd@glasgow.ac.uk.
authors.forename: Andrew J
authors.initials: AJ
authors.lastname: Todd
mesh_terms: D000818:Animals; D006801:Humans; D007395:Interneurons / Q000502:physiology; D009433:Neural Inhibition / Q000502:physiology*; D009473:Neuronal Plasticity / Q000502:physiology*; D010146:Pain / Q000503:physiopathology*; D059348:Peripheral Nerve Injuries / Q000503:physiopathology; D013116:Spinal Cord / Q000502:physiology*; D009435:Synaptic Transmission; D005680:gamma-Aminobutyric Acid / Q000502:physiology
chemical_list: D005680:gamma-Aminobutyric Acid