The　high　levels　of　glutamate　might　involve　in　neurogenesis　after　brain　injuries.　However,　the　mechanisms　are　not　fully　understood.　In　this　study,　we　investigated　the　effect　of　glutamate　on　the　proliferation　of　rat　embryonic　neural　stem/progenitor　cells　(NSCs)　through　regulating　the　vascular　endothelial　growth　factor　(VEGF)　expression　of　astrocytes　(ASTs)　in　vitro,　and　the　cyclin　D1　expression　of　NSCs.　The　results　showed　that　glutamate　promoted　the　expression　and　secretion　of　VEGF　of　rat　astrocytes　by　activating　group　I　mGluRs.　Astrocyte　conditioned　medium-containing　Glu　[ACM　(30%)]　promoted　the　proliferation　of　embryonic　NSCs　compared　with　normal　astrocyte　conditioned　medium+　Glu　[N-ACM　(30%)+　Glu　(30　mu　M)]　by　increasing　cell　activity,　diameter　of　neurospheres,　bromodeoxyuridine　(BrdU)　incorporation　and　cell　division;　while　ACM+　VEGF　neutralizing　antibody　[ACM　(30%)+　VEGF　NAb　(15　mu　g/ml)]　significantly　inhibited　the　proliferation　of　embryonic　NSCs　compared　with　ACM　(30%).　ACM　(30%)　increased　the　expressions　of　cyclin　D1　and　decreased　cell　death　compared　with　N-ACM　(30%)+　Glu　(30　mu　M).　ACM　(30%)+　VEGF　NAb　(15　mu　g/ml)　decreased　the　expressions　of　cyclin　D1　and　increased　cell　death　compared　with　ACM　(30%).　These　results　demonstrated　that　glutamate　could　also　indirectly　promote　the　proliferation　of　rat　embryonic　NSCs　through　inducing　the　VEGF　expression　of　ASTs　in　vitro,　and　VEGF　may　increase　the　expression　of　cyclin　D1.　These　finding　suggest　that　glutamate　may　be　a　major　molecule　for　regulating　embryonic　NSC　proliferation　and　facilitate　neural　repair　in　the　process　of　NSC　transplants　after　brain　injuries.