Effect of p75 neurotrophin receptor antagonist on disease progression in transgenic amyotrophic lateral sclerosis mice.

Neurotrophin level imbalances and altered p75 neurotrophin receptor (p75(NTR)) expression are implicated in spinal motor neuron degeneration in human and mouse models of amyotrophic lateral sclerosis (ALS). Recently, elevated reactive astrocyte-derived nerve growth factor (NGF) was linked to p75(NTR)-expressing motor neuron death in adult transgenic ALS mice. To test the role of NGF-dependent p75(NTR)-mediated signalling in ALS, we examined the effects of a cyclic decapeptide antagonist of p75(NTR) ligand binding by using neurotrophin-stimulated cell death assays and transgenic ALS mice.

Isolation and culture of motor neurons from the newborn mouse spinal cord.

A protocol for the isolation and culture of motor neurons from postnatal day 1 mouse spinal cord is described. After 72 h in culture, phase contrast microscopy reveals healthy cells with motor neuronal morphology and extensive neuritic processes. These neurons express the 75-kDa low-affinity neurotrophin receptor (p75NTR) and choline acetyltransferase (ChAT), both proteins are specifically expressed by neonatal and embryonic motor neurons in vivo.