Pre-treatment with lidocaine suppresses ectopic discharges and attenuates neuropeptide Y and c-Fos expressions in the rat cuneate nucleus following median nerve transection

Nitric Oxide Implicates c-Fos Expression in the Cuneate Nucleus Following Electrical Stimulation of the Transected Median Nerve

“…# P \ 0.05, ## P \ 0.01, ### P \ 0.001 compared with other groups by one-way ANOVA with Tukey's post hoc test discharges may primarily correlate with an abnormal activation of sodium channels in the injured nerve [36][37][38]. Our recent study further showed that a single local application of lidocaine prior to MNT could dose-dependently suppress the rate of injury discharges not only at the transection stage but also at all the other surveyed stages [23]. Of note, this study is the first to demonstrate that the amounts of NOS-LI neurons in the DRG and CN at 4 weeks after MNT were both dose-dependently reduced by lidocaine treatment prior to transection.…”

“…Thus, the variable sensitivity of anti-NOS antibodies employed might result in this Electrophysiological studies have demonstrated that peripheral nerve injury usually triggers injury discharges generating from the lesioned nerve fibers and their DRG [34,35]. Our previous study also showed that the rate of injury discharges peaked at the transection stage (a 10 min period immediately after nerve transection), which is considered to be a critical point for the development of ectopic discharges from injured nerves [23]. Several studies have demonstrated that ectopic discharge could be suppressed by lidocaine (a sodium channel blocker and local anesthetic), suggesting that the mechanism of ectopic Fig.…”

“…The above medulla and DRG sections were collected and treated with 0.5% (v/v) H 2 O 2 in PB for 30 min, washed and blocked with 5% (v/v) normal goat serum (GibcoBRL, Auckland, New Zealand) in PB, and then incubated for 48 h at 4°C with the following primary antibodies, diluted in 0.1 M PB containing 5% normal goat serum and 0.2% (v/v) Triton X-100: rabbit polyclonal anti-nNOS (1:2,000, Sigma), rabbit polyclonal anti-NPY (1:2000, Peninsula, San Carlos, CA, USA) [17,22] or c-Fos (1:2000, Calbiochem, San Diego, CA, USA) [3,23,24,32]. After several rinses with PB, the sections were incubated with biotinylated anti-rabbit IgG (1:200, Vector, Burlingame, CA, USA) for 2 h, and with an avidin-biotin horseradish peroxidase kit (ABC-HRP; Vector) for 1 h at room temperature.…”

“…It was demonstrated that the origin of the induced NPY-LI fibers in the CN was exclusively derived from the injured DRG neurons via primary afferent terminals (PATs) [22]. Furthermore, the results of pharmacological and morphological studies [23][24][25] have also shown that injury-induced NPY released from the injured median primary afferent terminals by electrical stimulation to significantly evoke c-Fos expression in the CTNs. The expressions of the proto-oncogene c-Fos and its protein product c-Fos have been widely used as a marker of neuronal activity, and as a neuronal marker of pain following noxious stimulation [26,27].…”

“…According to recent studies, median nerve injury-induced ectopic discharges, tactile hypersensitivity, and expression of NPY and c-Fos could be attenuated by application of lidocaine (a sodium channel blocker and local anesthetic) [23,31]. Thus, we sought to ascertain whether a single local application of lidocaine prior to MNT would alter the nNOS expression in the two above-mentioned regions.…”