A long T10–元 laminectomy was performed, and the dura mater was incised and retracted. The experimental setup and procedure are illustrated in the schematic diagram ( figs. Our observations suggest that dorsal column and root stimulation both attenuate the established WDR neuronal hyperexcitability in nerve-injured rats and suppress the short-term spinal neuronal sensitization in sham-operated rats. 18For the first time, antidromic compound APs in the sciatic nerve were recorded to standardize conditioning stimulation intensities ( i.e. , selective activation of Aα/β-fibers). Because of the evolving nature of anatomic and functional changes in the nervous system and changes in the efficacy of analgesics after nerve injury, 14–20we examined rats both at the peak of neuropathic pain (14–16 days postinjury) and at a later maintenance-recovery phase (45–75 days postinjury). This experimental paradigm allowed us to examine the respective effects of antidromic and orthodromic activation of large afferent fibers on spontaneous activity and the evoked responses of WDR neurons to mechanical stimuli, graded intracutaneous electrical stimuli, and windup-inducing electrical stimulation. Here, we applied a bipolar electrical stimulus to the thoracic dorsal column and the lumbar roots to compare how conditioning stimulation at a site that is rostral (dorsal column) or caudal (dorsal root) to the area where epidural spinal cord stimulation leads are usually placed in patients may differently affect lumbar WDR neuronal activity. 10–13Electrophysiologic studies in preclinical neuropathic pain models represent an important approach to studying the neurophysiologic mechanisms of spinal cord stimulation. 10–12Although windup is different from the longer lasting central sensitization, it is a useful experimental model for studying mechanisms that may contribute to initiating persistent pain. 7–9The action potential (AP) windup phenomenon in WDR neurons reflects an activity-dependent short-term increase in neuronal excitability. ![]() 6Wide dynamic range (WDR) neurons in the dorsal horn are important for spinal pain processing and are candidates for the “transmission” cells in the gate theory. Spinal cord stimulation was developed as a therapeutic modality based on the gate-control theory in which activation of afferent A fibers is postulated to attenuate spinal pain transmission. Because the electrical field of epidural stimulation may spread to nearby tissues via highly conductive cerebrospinal fluid, many action sites for spinal cord stimulation–induced pain relief may exist, but they have not been clearly defined. The class and number of nerve fibers that are activated under each circumstance are also unknown. 4,5It is unclear how paresthesia intensity correlates with the motor threshold. For example, bipolar stimulation that induces paresthesia that covers the painful areas is commonly used in patients, whereas monopolar stimulation at 60–90% of muscle twitching intensity ( i.e. , motor threshold) is often employed in experimental animals. Differences in lead design, stimulation mode, and intensity-selecting criteria also present barriers to correlating previous findings in experimental animals with mechanisms underlying therapeutic effects in patients. 1–3Yet, the biologic basis for the effectiveness of spinal cord stimulation in treating neuropathic pain is unclear. SPINAL cord stimulation is an effective neuromodulatory technique for managing a variety of chronic pain conditions, particularly neuropathic pain, which is often refractory to current pharmacotherapies. Therefore, stimulation of putative spinal substrates at A-fiber intensities with parameters similar to those used by patients with spinal cord stimulators attenuated established WDR neuronal hyperexcitability in the neuropathic condition and counteracted activity-dependent increase in neuronal excitability (i.e., windup). It is noteworthy that dorsal column stimulation blocked windup of WDR neuronal response to repetitive intracutaneous electrical stimulation (0.5 Hz) in nerve-injured and sham-operated rats, whereas dorsal root stimulation inhibited windup only in sham-operated rats. Conditioning stimulation also significantly attenuated WDR neuronal responses to mechanical stimuli in nerve-injured rats and inhibited the C-component of the neuronal response to graded intracutaneous electrical stimuli applied to the receptive field in nerve-injured and sham-operated rats. ![]() Within 15 min of the dorsal column or root conditioning stimulation, the spontaneous activity rate of WDR neurons was significantly reduced in nerve-injured rats.
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