Cisplatin is a carcinogenic agent having important cytotoxic effects. Cisplatin treatment increases the levels of free oxygen radicals in neurologic tissues. We investigated the effects of alpha lipoic acid (ALA) and melatonin (MEL) on the electrophysiological parameters and on activities of nerve fibers having different conduction properties on cisplatin neurotoxicity. Neurotoxicity was induced by a single injection of 10 mg/kg intraperitoneal (ip) cisplatin. Supplementation was started 1 day before cisplatin injection with either 100 mg/kg/day ip ALA or 4 mg/kg/day ip MEL for 7 days. Compound action potentials were recorded from isolated sciatic nerves in vitro, and numerical analyses were conducted. Cisplatin-induced neurotoxicity resulted in a significant decrease (p <.05) in maximum depolarization (mV), areas (mV·ms), and maximum and minimum upstroke velocity values (mV/ms). Although these decrements were restored by ALA and MEL, ALA was found to be more effective. Conventional conduction velocity measurements and conduction velocity distribution histograms have shown that ALA supplementation can recover the effects of cisplatin while MEL cannot. The conduction velocity distribution histograms have shown that antioxidant supplementation results in a restoration on contribution of fast-conducting fibers (51.8–77.7 m/s), which is deteriorated by cisplatin. Consequently, ALA has more potential to make up for the deleterious effects of cisplatin-induced neurotoxicity.

The aim of this study was to document the effect of tramadol as an opioid on individual fibers of rat sciatic nerve. To accomplish this objective, compound action potentials (CAPs) were recorded from isolated nerves treated with tramadol from five different concentration levels. Then recorded CAPs and the control group were analyzed by numerical methods namely Conduction Velocity Distribution (CVD) and Fast Fourier Transform (FFT). The results show that the area under CAP and the time derivative of CAP curves decreases, and the excitability of the nerve trunk falls as well (rheobase and chronaxie increases) with increasing tramadol concentration. CVD deduced by model study was divided into subgroups as SLOW (8-26 m/s), MODERATE (26-44 m/s), MEDIUM (44-60 m/s) and FAST (60-78 m/s). The decrement in percentage relative contribution of these conduction velocity groups starts with a concentration of 0.25 mM tramadol, especially in the subgroup named FAST. The power spectrum shifts from higher frequency region to lower frequency region as the tramadol concentration increases. These findings show that fast conducting fibers are more susceptible to tramadol than medium and moderate groups and tramadol possibly acts on channel activity rather than passive properties (such as space and time constant) of nerve fibers.

Gender differences, either with the structural or through with hormones, dictate how the corresponding organ or organ system responses to physiological signals. Current study aims to investigate gender dependent differences in conduction related parameters of rat sciatic nerve. Compound action potentials (CAP) were recorded via suction electrode whereas the conduction velocity distributions (CVD) were performed using the method known as collision technique in the literature. Studied CAP parameters, namely conduction velocities (CV), area of the CAPs and time required to reach the maximum depolarization (TP) have been found significantly different for female and male rats. Detailed analyses have shown that sex dependent differences were more remarkable in the right leg responses of female and male rats. Additionally, CVDs indicate that the number of fibers having CVs between 5-30 m/s is much more in male right sciatic nerve trunk when compared to age matched female rats. The present study, for the first time clearly shows that shift in the contribution of nerve fibers to lower CVs is the main causal of the sex dependent differences seen in rat sciatic nerve fibers.

Cardiac dysfunction is secondary to acute mesenteric ischemia (AMI) and abdominal aortic aneurysms (AAA). The underlying cause of distant organ damage in the heart is the formation of oxidative stress caused by ischemia-reperfusion. In this study, we investigated the possible protective effects of a novel mitochondria-targeted antioxidant MitoTEMPO on contractile dysfunction and structural defects of the rat papillary muscle caused by abdominal ischemia-reperfusion (AIR). In the experiments, adult Wistar-Albino rats were used and animals were divided randomly into 3 groups; sham-operated group (SHAM), an IR group that had aortic cross-clamping for 1 h followed by 2 h reperfusion, and a third group that received protective 0.7 mg/kg/day MitoTEMPO injection for 28-day before IR. As a result, it was observed that MitoTEMPO injection had a protective effect on the mechanical activities and structural properties of the papillary muscle impaired by AIR. Our study also showed that AIR disrupted the contractile function of the papillary muscle for each stimulation frequency and post-potentiation responses tested. This is common for each measured and calculated mechanical parameter and MitoTEMPO injection showed its protective effects. Consequently, calcium homeostasis seems to be impaired by AIR, and MitoTEMPO may exert its protective effect through energy metabolism by directly targeting the mitochondria.