Persistent hindlimb inflammation induces changes in activation properties of hyperpolarization-activated current (Ih) in rat C-fiber nociceptors in vivo.

摘要: A hallmark of chronic inflammation is hypersensitivity to noxious and innocuous stimuli. This inflammatory pain results partly from hyperexcitability nociceptive dorsal root ganglion (DRG) neurons innervating inflamed tissue, although the underlying ionic mechanisms are not fully understood. However, we have previously shown that nociceptor associated with increased expression hyperpolarization-activated cyclic nucleotide-gated channel 2 (HCN2) protein current (Ih) in C-nociceptors. Here used vivo voltage-clamp current-clamp recordings, deeply anesthetized rats, determine whether activation properties Ih these C-nociceptors also change following persistent (not acute) hindlimb induced by complete Freund's adjuvant (CFA). Recordings were made lumbar (L4/L5) C-nociceptive DRG neurons. Behavioral sensory testing was performed 5-7days after CFA treatment, all CFA-treated group showed significant behavioral signs mechanical heat hypersensitivity, but spontaneous pain. Compared control, recorded showed: (a) a increase incidence activity (from ∼5% 26%) albeit at low rate (0.14±0.08Hz (Mean±SEM); range, 0.01-0.29Hz), (b) percentage expressing 35%, n=43-84%, n=50) based on presence voltage "sag" >10%, (c) conductance (Gh) somatic channels conducting along corresponding Ih,Ih, rate, dependence, Given depolarizes neuronal membrane toward threshold action potential generation, changes kinetics may contribute their thus inflammation.