Reduction in inflammation-induced sensitization of dorsal horn neurons by transcutaneous electrical nerve stimulation in anesthetized rats

Abstract

Transcutaneous electrical nerve stimulation (TENS) is utilized to treat a variety of painful conditions. Inflamed animals present with an increased response to noxious stimuli, i.e., hyperalgesia, at the site of injury (primary hyperalgesia) and outside the site of injury (secondary hyperalgesia). Further, following acute inflammation, dorsal horn neurons show an increased responsiveness to peripherally applied stimuli, which has been termed sensitization. Previous studies demonstrate a reduction in dorsal horn neuron activity following TENS treatment in normal animals and a reduction in primary and secondary hyperalgesia in acutely inflamed animals. The purpose of this study was to examine the effects of TENS on dorsal horn neurons sensitized by acute inflammation. Extracellular recordings from wide dynamic range (WDR), high threshold (HT) and low threshold (LT) dorsal horn neurons in anesthetized rats were assessed for spontaneous activity, responses to innocuous and noxious mechanical stimulation and receptive field size. Responses were measured before and 3 h after induction of inflammation, and immediately and 1 h after application of either high (100 Hz) or low (4 Hz) frequency TENS (motor intensity, pulse duration = 100 microseconds). TENS was applied to the inflamed paw to encompass the receptive field of the neuron for 20 min. WDR and HT dorsal horn neurons sensitized to mechanical stimulation after induction of inflammation. Application of either high or low frequency TENS to the inflamed paw reduced both innocuous and noxious evoked responses of WDR and HT dorsal horn neurons immediately and 1 h after treatment with TENS. Comparison of responses after TENS with baseline responses showed that the evoked responses in the majority of WDR and HT cells returned to or fell below baseline responses. TENS had no effect on responses of LT neurons. In summary, central neuron sensitization is reduced by TENS and may underlie the reduction in hyperalgesia observed after treatment with TENS.

Release of GABA and activation of GABAA in the spinal cord mediates the effects of TENS in rats

“…The delayed increases in extracellular GABA in the spinal cord in response to TENS parallel the timing of TENS antihyperalgesia testing in prior studies (Sluka et al, 1998). In addition to antihyperalgesia occurring after removal of TENS, inhibition of dorsal horn neuron sensitization also continues after removal of TENS (Ma and Sluka, 2001). Thus, delayed increases in GABA follow the time course of effectiveness of high frequency TENS for reduction in hyperalgesia and thus likely represent one mechanism by which TENS reduces pain.…”

Basic Understanding of Transcutaneous Electrical Nerve Stimulation

“…6,11) A number of basic scientific studies proved that TENS could inhibit the central transmission of nociceptive impulses through the involvement of endogenous opioids, gamma-amino butyric acid (GABA), acetylcholine, 5-HT, noradrenaline and adenosine at peripheral, spinal or supraspinal (brainstem) sites levels. [12][13][14][15] Moreover, clinical experience suggests that TENS is still beneficial for various pains with neuropathic, nociceptive or musculoskeletal origin and popular with patients as well as clinician. 11) Taken together, it is still supported that clinicians continue to offer patients TENS until enough evidences with better quality will be provided.…”

Extracellular currents alter gap junction intercellular communication in synovial fibroblasts

“…Exposure to low frequency electromagnetic fields (EMFs) has been reported to ameliorate pain perception in patients [Stone and Wharton, 1997;Pridmore and Oberoi, 2000;Hurley et al, 2001;Lefaucheur et al, 2001] and in various animal models [Leem et al, 1995;Prato et al, 1995;Jeong et al, 2000;Ma and Sluka, 2001], but little is known about the responsible mechanisms. One possibility is that the EMFs produced analgesia by directly affecting the cells of the nervous system.…”