OBJECTIVE: To determine whether activation and/or inhibition of α-adrenoreceptors influences substance P (SP) release from dorsal root ganglion (DRG) primary sensory neurons in vitro. METHODS: DRGs were dissected from 15-day embryonic Wistar rats. DRG neurons were dissociated and cultured for 2 d and then exposed to noradrenaline (NA) alone (1×10(-4) mol/L), or along with the α1-adrenoreceptor antagonist prazosin (1×10(-6) mol/L) or the α2-adrenoreceptor antagonist yohimbine (1×10(-5) mol/L) for 4 d. Then, RT-PCR was used to determine the levels of preprotachykinin (PPT) mRNA encoding for SP and Western blot to assess the protein levels of SP. Basal and capsaicin (CAP)-evoked SP release were measured by enzyme-linked immunosorbent assay (ELISA). RESULTS: CAP-evoked SP release was sensitized by NA and this effect was inhibited by pre-incubation with prazosin but not with yohimbine. The levels of PPT mRNA, SP peptide, and basal SP release did not change significantly in any of the experimental conditions. CONCLUSION: NA may significantly increase CAP-evoked SP release through activation of α-adrenoreceptors, which may contribute to noradrenergic pain modulation.
OBJECTIVE: To determine whether activation and/or inhibition of α-adrenoreceptors influences substance P (SP) release from dorsal root ganglion (DRG) primary sensory neurons in vitro. METHODS: DRGs were dissected from 15-day embryonic Wistar rats. DRG neurons were dissociated and cultured for 2 d and then exposed to noradrenaline (NA) alone (1×10(-4) mol/L), or along with the α1-adrenoreceptor antagonist prazosin (1×10(-6) mol/L) or the α2-adrenoreceptor antagonist yohimbine (1×10(-5) mol/L) for 4 d. Then, RT-PCR was used to determine the levels of preprotachykinin (PPT) mRNA encoding for SP and Western blot to assess the protein levels of SP. Basal and capsaicin (CAP)-evoked SP release were measured by enzyme-linked immunosorbent assay (ELISA). RESULTS:CAP-evoked SP release was sensitized by NA and this effect was inhibited by pre-incubation with prazosin but not with yohimbine. The levels of PPT mRNA, SP peptide, and basal SP release did not change significantly in any of the experimental conditions. CONCLUSION: NA may significantly increase CAP-evoked SP release through activation of α-adrenoreceptors, which may contribute to noradrenergic pain modulation.