MOLECULAR PAIN

Cystitis induces considerable changes in the primary af-ferent pathways that play a significant role in bladder hyperactivity. The molecular mechanism and signal transduction that mediate the cross talk between the inflamed urinary bladder and sensory sensitization has not been investigated. The neuropeptide calcitonin gene-related peptide (CGRP) is enriched in the primary afferent neurons in the dorsal root ganglia (DRG) and is one of the most important nociceptive markers in the control of pain and inflammation [1-10]. Mice lacking CGRP or receiving pharmacological inhibition of CGRP activity do not develop hyperalgesia or central neuro-pathic pain after inflammation [4-10]. Conversely, mice receiving intrathecal CGRP peptide exhibit nociceptive behavior [11-13]. The involvement of CGRP in nocicep