Neuroprotective effect of l-serine against white matter demyelination by harnessing and modulating inflammation in mice.

Demyelination in white matter is the end product of numerous pathological processes. This study was designed to evaluate the neuroprotective effect of l-serine and the underlying mechanisms against the demyelinating injury of white matter. A model of focal demyelinating lesions (FDL) was established using the two-point stereotactic injection of 0.

A stable and easily reproducible model of focal white matter demyelination.

Background: Demyelination is the end product of numerous pathological processes, and also is one of the main causes of neurological disability in Multiple sclerosis (MS). Research into the pathogenesis of MS is hampered by the conventional rodent models' inability to produce stable demyelination.

New Method: Focal demyelinating lesions were stereotactically targeted to the corpus callosum with a two-point injection of lysophosphatidylcholine (LPC-2) in mice.

TRPC6 inhibited NMDA current in cultured hippocampal neurons.

N-methyl-D-aspartate (NMDA) receptors play a key role in excitatory synaptic transmission, plasticity and neural development, and they also mediate excitotoxicity that is involved in both acute neuronal damage and chronic neurodegenerative diseases. Regulation of the NMDA channel activity is critical for the pathological processes of these diseases. The canonical transient receptor potential channels (TRPCs) are Ca(2+)-permeable nonselective cation channels with various physiological functions, including promoting neuronal survival.