A novel molecular mechanism linking a neurotrophin with a Toll-family and kinase-less Trk-like receptors provides a direct link from molecules to structural circuit plasticity and modification of behaviour.
RNA-Seq analysis and molecular biological approaches reveal a novel mechanism and provide a promising preventive and therapeutic molecular target for vulnerability to chronic pain-related memory impairment.
The important role of structural asymmetry in the functional lateralization of the same brain area provides a crucial insight into the neurobiological fundament for human brain's functional lateralization.
Aging reduces the potassium M current in sympathetic motor neurons, resulting in a hyperactive phenotype that can be reversed by pharmacological activation of these channels.
