Inhibition of neuronal FLT3 receptor tyrosine kinase alleviates peripheral neuropathic pain in mice.

Peripheral neuropathic pain (PNP) is a debilitating and intractable chronic disease, for which sensitization of somatosensory neurons present in dorsal root ganglia that project to the dorsal spinal cord is a key physiopathological process. Here, we show that hematopoietic cells present at the nerve injury site express the cytokine FL, the ligand of fms-like tyrosine kinase 3 receptor (FLT3). FLT3 activation by intra-sciatic nerve injection of FL is sufficient to produce pain hypersensitivity, activate PNP-associated gene expression and generate short-term and long-term sensitization of sensory neurons.

Early functional outcomes and histological analysis after spinal cord compression injury in rats.

Object: Neuroprotective and repair strategies in spinal cord injuries (SCIs) have been so far largely unsuccessful. One of the prerequisites is the use of appropriate preclinical models to decipher pathophysiological mechanisms; another is the identification of optimal time windows for therapeutic interventions. The authors undertook this study to characterize early motor, sensory, autonomic, and histological outcomes after balloon compression of the spinal cord at the T8-9 level in adult rats.

A remotely controlled model of spinal cord compression injury in mice: toward real-time analysis.

Object: To date, there has been no efficient therapeutic approach to spinal cord injuries (SCIs). This may be attributable, at least in part, to difficulties in forming predictive and accurate experimental animal models. The authors' previous studies have identified 2 relevant conditions of such a model.

Minimum information about animal experiments: supplier is also important.

It has now been established that functional recovery after spinal cord injury (SCI) depends on several parameters, including animal strain. Here we demonstrate that rats from the same strain (Wistar) but from two independent commercial suppliers present different motor, sensory, and autonomic outcomes after a standard model of SCI, the so-called compression model. Recovery is correlated with the extension of the lesion, and we show that the vertebral canal diameter varies between the two suppliers.

Time course of acute phase in mouse spinal cord injury monitored by ex vivo quantitative MRI.

During the acute phase of spinal cord injury (SCI), major alterations of white and grey matter are a key issue, which determine the neurological outcome. The present study with ex vivo quantitative high-field magnetic resonance microimaging (MRI) was intended in order to identify sensitive parameters of tissue disruption in a well-controlled mouse model of ischemic SCI. MR imaging evidenced changes as early as the second hour after the lesion in the dorsal horns, which appear swollen.

A mouse model of acute ischemic spinal cord injury.

Mice models of spinal cord injury (SCI) should improve our knowledge of the mechanisms of injury and repair of the nervous tissue. They represent a powerful tool for the development of therapeutic strategies in the fields of pharmacological, cellular, and genetic approaches of neurotrauma. We demonstrate here that the photochemical graded ischemic spinal cord injury model, described in rats, can be successfully adapted in mice, in a reliable and reproducible manner.