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Abstract

Peripheral nervous system alterations were induced in adult rats by administration of cisplatin (CDDP) 2 mg/kg twice weekly for 4.5 weeks. Dorsal root ganglion neurons showed pathological changes. Morphometric determinations demonstrated a reduction in size of the somatic, nuclear and nucleolar area. The nucleoli were the most involved subcellular structures. Nerve conduction velocity and the tail-flick test for pain were both significantly altered in CDDP treated rats, whereas the rota-rod test for coordination revealed no changes in either treated or control rats. Analytical determinations demonstrated platinum accumulation in the DRG of CDDP treated rats. Spontaneous recovery, demonstrated by morphometric, electrophysiological, functional and analytical determinations, occurred after treatment discontinuation within about 7 weeks. A pilot study of the possible neuroprotective action of retinoic acid (RA) was also performed with this model of cisplatin neuronopathy. The rationale for using RA was based on its assumed antioxidant and neurotrophic effect. However, RA failed to prevent morphometric, electrophysiological, functional and analytical alterations induced by CDDP on DRG neurons. RA induced only a mild generalized protective effect.

Cannabinoid Type-1 Receptor Reduces Pain and Neurotoxicity Produced by Chemotherapy

“…Consistent with earlier clinical (Cooley et al, 1994; Sleijfer et al, 1985) and experimental (Tredici et al, 1998; Joseph and Levine, 2009; Ta et al, 2009) reports, mechanical and heat hyperalgesia occurred in the majority of mice treated with cisplatin in the present study. Because cisplatin does not cross the blood-brain barrier (Gregg et al, 1992) and no obvious deterioration in general health or motor activity occurred during the 7-day course of treatment, the hyperalgesia observed in cisplatin-treated mice is most likely due to changes in sensory neurons.…”

Erythropoietin both protects from and reverses experimental diabetic neuropathy

“…Antidromic tail-nerve conduction velocity was assessed by using a Myto EBNeuro electromiograph (EBNeuro, Firenze, Italy), as described (24). The latency of potential recorded in the two sites after nerve stimulation (stimulus duration, 100 msec; filter, 1 Hz to Ϫ5 MHz) was determined (peak to peak), and NCV was calculated accordingly.…”

A ruthenium(II) complex inhibits tumor growth in vivo with fewer side-effects compared with cisplatin

“…The latency to lick a hind paw was measured. The mice were removed from the plate immediately upon licking a hind paw or if no response occurred within 50 s. At the same time, the rotarod test was employed to assess peripheral motor nerve toxicity [33,34]. The mice were trained to remain on the rotarod apparatus (YLS-4C, ZS Dichuang Inst, Peking, China) before the experimental data were obtained.…”

“…These results indicated that cisplatin significantly injured the sensory nerve, whereas Δ-Ru1 showed no toxicity toward it. The rotarod test was used to evaluate coordination, which if altered, could indicate peripheral motor neurotoxicity [33]. In the rotarod test, the time that the animal spent on the rotating drum was measured (Fig.…”