Increase in extracellular potassium level in rat spinal dorsal horn induced by noxious stimulation and peripheral injury

Optically Recorded Response of the Superficial Dorsal Horn: Dissociation From Neuronal Activity, Sensitivity to Formalin-Evoked Skin Nociceptor Activation

“…4). This observation is in accord with the report (Svoboda et al 1988) that, in normal subjects, [K ϩ ] o is maintained at lower values in the superficial dorsal horn (laminae I-II) than in the deeper laminae (laminae III-V) and raises the possibility that the capacity of laminae I-II astocytes to take up K ϩ and GLU (along with water) may be greater than that of layer IV astrocytes. Interestingly, a differential capacity of astrocytes in the superficial versus deep dorsal horn to take up K ϩ and GLU would be compatible with recent demonstrations that K ϩ channels and aquaporins tend to colocalize in astrocyte membranes, and aquaporin expression is higher in the superficial dorsal horn than in the deeper laminae (Asai et al 2002;see also Binder et al 2004).…”

“…We regarded multiple lines of published evidence as consistent with the possibility that the vigorous C-nociceptor activity evoked by algesic chemical to skin or muscle (Klemm et al 1989;McCall et al 1996;Porro et al 2003;Puig and Sorkin 1996) is accompanied by an impaired ability of astrocytes to regulate dorsal horn extracellular fluid composition. First, intracutaneous formalin injection is accompanied by a large and prolonged elevation of [K ϩ ] o in the superficial dorsal horn (Heinemann et al 1990;Svoboda et al 1988). Second, tetanic nerve stimulation, noxious skin stimulation, inflammation, or an experimentally imposed elevation of dorsal horn [K ϩ ] o is followed by long-term changes in the efficacy of C-fiber-mediated synaptic activation of dorsal horn neurons (Ma and Zhao 2002;Sandkuhler and Liu 1998;Sandkuhler et al 2000; for CNS effects of elevated [K ϩ ] o , see Somjen 2002).…”

“…Second, tetanic nerve stimulation, noxious skin stimulation, inflammation, or an experimentally imposed elevation of dorsal horn [K ϩ ] o is followed by long-term changes in the efficacy of C-fiber-mediated synaptic activation of dorsal horn neurons (Ma and Zhao 2002;Sandkuhler and Liu 1998;Sandkuhler et al 2000; for CNS effects of elevated [K ϩ ] o , see Somjen 2002). Third, the hyperalgesia/ persistent pain, glial activation, and the abnormal elevation of dorsal horn [K ϩ ] o that develop after intracutaneous formalin injection are either prevented entirely or substantially reduced by prior local anesthetic block of action potential conduction in the afferents that innervate the injection site (Fu et al 2000;Svoboda et al 1988).…”

Potentiation of P2Y Receptors by Physiological Elevations of Extracellular K+via a Mechanism Independent of Ca2+Influx

“…P2Y 1 receptors are located in several cardiovascular tissues, including the heart, endothelium, and vascular smooth muscle; the effect we observe here could therefore play a widespread role in adaptations to exercise. P2Y 1 receptors are also located in sensory ganglia (Ruan and Burnstock, 2003), and both noxious stimuli and painful injury are known to evoke a sustained increase in [K ϩ ] o of up to 3 mM (Svoboda et al, 1988). Therefore, the K ϩ dependence of the P2Y 1 receptor [or other P2Y subtypes expressed in these ganglia (Moriyama et al, 2003) and exhibiting a dependence upon [K ϩ ] o ] could have relevance to the mechanisms underlying neuropathic pain.…”

Role of glia in K+ and pH homeostasis in the neonatal rat spinal cord

“…quency of 10 Hz and by 2.5-3.5 mM at 30 Hz when the K+ ceiling level is achieved (Svoboda et al, 1988). The transient pH, changes during repetitive stimulation are dominated by an acid shift of 0.1-0.2 pH units that is preceded by an initial alkaline shift of about 0.005 pH units (Sykova and Svoboda, 1990).…”