Abstract
Glioblastoma cells release and exploit glutamate for proliferation and migration by autocrine or paracrine loops through Ca2+ -permeable・-amino-3-hydroxy-5-methyl-4-isoxazolepropionate -type glutamate receptors (CP-AMPAR). Here we show the molecular mechanism behind glioblastoma cells expressing CP-AMPAR, and refer to its role for gliomagenesis.