The long term goals of this project are to understand the neurophysiology of low back pain including the relative effectiveness of pharmacologic treatment modalities. The initial studies will focus on peripheral innervation and neurophysiology of spinal canal structures. Later studies will include higher order neurons, with recordings made at dorsal horn, thalamus and somatosensory cortex. The spinal canal structures to be studied include disc, posterior longitudinal ligament, ventral dura, dorsal roots and dorsal root ganglia. These tissues have long been suspected to be sources of low back pain, but their innervation has never been characterized neurophysiologically. The purpose of this proposal is to determine how the somatosensory neurons of these tissues respond to mechanical stress and strain and chemical mediators of pain and inflammation. The model we will use is the New England White rabbit. Specific Aims: 1. Determine the neuronal response of lumbar intervertebral discs, posterior longitudinal ligaments, ventral dura, dorsal roots and dorsal root ganglia to local mechanical stress. 2. Determine the neuronal response of the intervertebral disc to disc loading. 3. Determine the response of these same tissues to exposure to proven and hypothesized chemical mediators of inflammation, including herniated nucleus pulposus, phospholipase A2, substance P, bradykinin and serotonin. 4. Determine the nerve distribution of somatosensory neuropeptides in these tissues. Hypotheses: 1. That low back pain can be caused by mechanical or chemical stimulation of nociceptors in the annulus of the discs, posterior longitudinal ligament or ventral dura. This hypothesis has never been demonstrated neurophysiologically. 2. That low back pain and sciatica can be caused by mechanical stress or inflammation of lumbar dorsal roots and/or dorsal root ganglia.