Oxaliplatin-induced cold hypersensitivity is due to remodelling of ion channel expression in nociceptors.

Cold hypersensitivity is the hallmark of oxaliplatin-induced neuropathy, which develops in nearly all patients under this chemotherapy. To date, pain management strategies have failed to alleviate these symptoms, hence development of adapted analgesics is needed. Here, we report that oxaliplatin exaggerates cold perception in mice as well as in patients.

Phosphorylation of spinal N-methyl-d-aspartate receptor NR1 subunits by extracellular signal-regulated kinase in dorsal horn neurons and microglia contributes to diabetes-induced painful neuropathy.

The N-methyl-d-aspartate receptor (NMDAR) contributes to central sensitization in the spinal cord, a phenomenon which comprises various pathophysiological mechanisms responsible for neuropathic pain-like signs in animal models. NMDAR function is modulated by post-translational modifications including phosphorylation, and this is proposed to underlie its involvement in the production of pain hypersensitivity. As in diabetic patients, streptozotocin-induced diabetic rats exhibit or not somatic mechanical hyperalgesia; these rats were named DH and DNH respectively.

Quantitative and spatial differences in the expression of tryptophan-metabolizing enzymes in mouse epididymis.

Previous reports have suggested that indoleamine 2,3-dioxygenase (IDO) activity is particularly important in mouse epididymis tissue. We show here, using reverse transcription/polymerase chain reaction assays, Northern assays, Western blotting experiments, and immunohistochemistry that IDO is indeed highly expressed in mouse epididymis, and that IDO mRNA distribution and protein location are precisely regionalized within the organ and within sub-territories of the proximal part of the epididymal duct, the so-called caput epididymidis. Within the caput epididymidis, both the principal and the apical cells have been shown to express IDO.