Vascular changes in the subventricular zone after distal cortical lesions

被引:45
作者
Gotts, JE
Chesselet, MF
机构
[1] Univ Calif Los Angeles, Geffen Sch Med, Dept Neurol, Los Angeles, CA 90095 USA
[2] Univ Calif Los Angeles, Geffen Sch Med, Dept Neurobiol, Los Angeles, CA 90095 USA
关键词
subventricular zone; rostral migratory stream; VEGF; neurogenesis; stem cells; alpha; 5; beta; 3; integrin;
D O I
10.1016/j.expneurol.2005.02.001
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
One of the effects of cortical lesions is to produce cell proliferation in the subventricular zone (SVZ), a neurogenic zone of the adult brain distal from the lesion. The mechanisms of these effects are unknown. Recent evidence points to a relationship between the vasculature and neurogenesis both in vitro and in vivo. In the present study, we asked whether cortical lesions induced vascular modifications in the distal SVZ in vivo. Lesions of the frontoparietal cortex were produced by thermocoagulation of pial blood vessels, a method that leads to highly reproducible loss of all cortical layers, sparing the corpus callosum and underlying striatum, These lesions induced increased immunoreactivity for vascular endothelial growth factor (VEGF) around the walls of SVZ vessels, at a considerable distance from the lesion. Vascular permeability was markedly increased in both the SVZ and RMS by 3 days after the injury. A dramatic increase in endothelial proliferation was followed by expansion of the local SVZ vascular tree 7 days after the injury. This time course corresponded to the proliferative changes in the SVZ, and a tight correlation was observed between the number of blood vessels and the increase in SVZ cell number. The data demonstrate that thermocoagulatory cortical lesions induce distal vascular changes that could play a role in lesion-induced SVZ expansion. (c) 2005 Elsevier Inc. All rights reserved.
引用
收藏
页码:139 / 150
页数:12
相关论文
共 64 条
[1]  
[Anonymous], LACTIC MICROFLORA PI
[2]   REQUIREMENT OF VASCULAR INTEGRIN ALPHA(V)BETA(3) FOR ANGIOGENESIS [J].
BROOKS, PC ;
CLARK, RAF ;
CHERESH, DA .
SCIENCE, 1994, 264 (5158) :569-571
[3]  
Burchardt M, 2000, PROSTATE, V43, P184, DOI 10.1002/(SICI)1097-0045(20000515)43:3<184::AID-PROS4>3.0.CO
[4]  
2-6
[5]  
Carmichael ST, 2002, J NEUROSCI, V22, P6062
[6]   Traumatic brain injury induced cell proliferation in the adult mammalian central nervous system [J].
Chirumamilla, S ;
Sun, D ;
Bullock, MR ;
Colello, RJ .
JOURNAL OF NEUROTRAUMA, 2002, 19 (06) :693-703
[7]   Increased blood-brain barrier permeability and endothelial abnormalities induced by vascular endothelial growth factor [J].
Dobrogowska, DH ;
Lossinsky, AS ;
Tarnawski, M ;
Vorbrodt, AW .
JOURNAL OF NEUROCYTOLOGY, 1998, 27 (03) :163-173
[8]  
DUIJVESTIJN AM, 1992, LAB INVEST, V66, P459
[9]   Vascular permeability factor/vascular endothelial growth factor: A critical cytokine in tumor angiogenesis and a potential target for diagnosis and therapy [J].
Dvorak, HF .
JOURNAL OF CLINICAL ONCOLOGY, 2002, 20 (21) :4368-4380
[10]   DEVELOPMENT OF A MICROMETHOD TO STUDY THE NA+-INDEPENDENT L-[H-3]GLUTAMIC ACID BINDING TO RAT STRIATAL MEMBRANES .2. EFFECTS OF SELECTIVE STRIATAL LESIONS AND DEAFFERENTATIONS [J].
ERRAMI, M ;
NIEOULLON, A .
BRAIN RESEARCH, 1986, 366 (1-2) :178-186