American Pain Society's 27th Annual Scientific Meeting (May 8 – 10, 2008): The Persistence of Pain: LTP, Central Sensitization, and Pain Memory

There have been recent advances in our appreciation of the impact of chronic pain on the lives of people, as well as the discovery of strikingly similar mechanisms related to learning and memory. Dr. Sandkühler will discuss the synaptic hypothesis of hyperalgesia postulating that hyperalgesia is induced by activity-dependent long-term potentiation (LTP) in the spinal cord, and the properties of a novel synaptic amplifier at the origin of an ascending pain pathway that is switched-on by low-level activity in nociceptive nerve fibers. Dr. Hains will describe pain-induced dendritic spine remodeling and redistribution that is analogous to cortical memory formation, which is governed by a single identified molecule (Rac1). He will present results demonstrating Rac1-mediated dendritic spine plasticity, enhancement of excitatory postsynaptic currents, and altered nociceptive processing, leading to behavioral pain phenotypes. Dr. Apkarian will discuss how pain and memory are intricately interrelated at the cortical level. Human brain imaging and behavioral data will be presented, and the reverse translation of these results into the animal setting will also be shown. The latter leads to testing new families of chemicals as potential tools with which the suffering of pain may be controlled. The clinical significance and treatment implications will be reviewed.