title: Spinal cord injury, dendritic spine remodeling, and spinal memory mechanisms.
abstract: Spinal cord injury (SCI) often results in the development of neuropathic pain, which can persist for months and years after injury. Although many aberrant changes to sensory processing contribute to the development of chronic pain, emerging evidence demonstrates that mechanisms similar to those underlying classical learning and memory can contribute to central sensitization, a phenomenon of amplified responsiveness to stimuli in nociceptive dorsal horn neurons. Notably, dendritic spines have emerged as major players in learning and memory, providing a structural substrate for how the nervous system modifies connections to form and store information. Until now, most information regarding dendritic spines has been obtained from studies in the brain. Recent experimental data in the spinal cord, however, demonstrate that Rac1-regulated dendritic spine remodeling occurs on second-order wide dynamic range neurons and accompanies neuropathic pain after SCI. Thus, SCI-induced synaptic potentiation engages a putative spinal memory mechanism. A compelling, novel possibility for pain research is that a synaptic model of long-term memory storage could explain the persistent nature of neuropathic pain. Such a conceptual bridge between pain and memory could guide the development of more effective strategies for treatment of chronic pain after injury to the nervous system.
authors.affiliation: Department of Neurology, Yale University School of Medicine, New Haven, CT 06510, USA.
authors.forename: Andrew M
authors.initials: AM
authors.lastname: Tan
authors.forename: Stephen G
authors.initials: SG
authors.lastname: Waxman
mesh_terms: D000818:Animals; D049229:Dendritic Spines / Q000502:physiology*; D008568:Memory / Q000502:physiology*; D009437:Neuralgia / Q000503:physiopathology; D009473:Neuronal Plasticity / Q000502:physiology*; D009474:Neurons / Q000502:physiology*; D013119:Spinal Cord Injuries / Q000503:physiopathology*; D013569:Synapses / Q000502:physiology