Fig. 5.
Knockdown of growth arrest and DNA-damage–inducible protein 45β (Gadd45β) expression restores nerve ligation-induced enhanced voltage-dependent T-type calcium channel 3.2 subunit (CaV3.2) currents in spinal dorsal horn neurons. (A) Representative traces of total voltage-dependent T-type currents (Total T-type currents) and CaV3.2 currents in spinal dorsal horn neurons on day 7 postoperation dissected from sham-operated (Sham 7D) and spinal nerve ligation (SNL 7D) rats as well as SNL rats treated with missense siRNA (SNL 7D + MS RNAi; 5 μg, 10 μl) and Gadd45β-targeting siRNA (SNL 7D + Gadd45β RNAi; 5 μg, 10 μl). l-Ascorbic acid, a CaV3.2 antagonist (300 μM). (B) The current–voltage (I–V) curves of CaV3.2-dependent currents in spinal dorsal horn neurons from sham (Sham 7D) and SNL rats (SNL 7D) and SNL rats treated with Gadd45β-targeting siRNA (SNL 7D + Gadd45β RNAi) or missense siRNA (SNL 7D + MS RNAi). When compared with the sham operation, SNL increases peak currents of the I–V curve that is reversed by that intrathecally daily application of Gadd45β-targeting siRNA but not the missense siRNA. (C) Peak values of the CaV3.2-dependent current densities (pA–pF) showing reduced the peak amplitude of CaV3.2 currents compared with SNL group. **P < 0.01 versus Sham 7D. ##P < 0.01 versus SNL 7D. n = 6. Data represent mean ± SD.