Changes in somatic action potential shape in guinea-pig nociceptive primary afferent neurones during inflammation in vivo

1. We have examined whether there are changes during inflammation in the me mbrane properties of nociceptive primary afferent neurones in the guinea-pi g that might contribute to hyperalgesia. Inflammation was induced by intrad ermal injections of complete Freund's adjuvant (CFA) in the left leg. Intra cellular voltage recordings were made from the somata of ipsilateral L6 and S1 dorsal root ganglion neurones in anaesthetised untreated guinea-pigs at 2 or 4 days after CFA treatment. 2. Units were classified as C, A delta or A alpha/beta on the basis of thei r dorsal root conduction velocities (CVs). Units with receptive fields on t he left leg were characterized as nociceptive, low-threshold mechanorecepti ve (LTM) or unresponsive according to their responses to mechanical and the rmal stimuli. The shapes of their somatic action potentials (APs) evoked by dorsal root stimulation were recorded. 3. Comparisons of data from nociceptive neurones recorded in CFA treated an imals after 2 and 4 days with data from CFA untreated (control) animals sho wed the following significant changes: in C-fibre nociceptors, decreased AP duration at base, AP rise time and AP fall time, and increased maximum rat es of AP rise and fall with no change in after-hyperpolarization measured t o 80 % recovery (AHP(80)); in A delta-fibre nociceptors, decreased AP durat ion at base, AP fall time and a reduction in AHP(80); and in A alpha/beta-f ibre nociceptors, a decreased AHP(80) but no change in AP duration. Apart f rom a more negative membrane potential and AHP depth below 0 mV in A alpha/ beta nociceptors at 4 days compared with 2 days post-CFA, none of the above variables differed significantly between units recorded 2 or 4 days after CFA. Therefore the two groups were pooled and called CFA2 + 4d. 4. The reduction in AP duration in C-fibre nociceptors was apparent both in high threshold mechanoreceptor and polymodal nociceptors and also in units with either cutaneous or subcutaneous receptive fields. 5. No significant changes in AP duration at base or AHP(80) were seen 2 or 4 days after CFA compared with control in either LTM or unresponsive neuron es, although some of the latter may have become classified as nociceptors a fter CFS treatment. 6. The alterations in membrane properties of nociceptors should permit high er discharge frequencies, thus contributing to inflammatory hyperalgesia. T hey suggest active changes in the expression or activation of cation channe ls during peripheral inflammation.