BDNF overexpression increases dendrite complexity in hippocampal dentate gyrus

被引:160
作者
Tolwani, RJ
Buckmaster, PS
Varma, S
Cosgaya, JM
Wu, Y
Suri, C
Shooter, EM
机构
[1] Stanford Univ, Dept Neurobiol, Sch Med, Stanford, CA 94305 USA
[2] Stanford Univ, Dept Comparat Med, Sch Med, Stanford, CA 94305 USA
[3] Regeneron Pharmaceut Inc, Tarrytown, NY 10591 USA
关键词
brain-derived neurotrophic factor; dendrite structure; granule cells; dentate gyrus; plasticity; TrkB receptor;
D O I
10.1016/S0306-4522(02)00301-9
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
There is increasing evidence that brain-derived neurotrophic factor (BDNF) modulates synaptic and morphological plasticity in the developing and mature nervous system. Plasticity may be modulated partially by BDNF's effects on dendritic structure. Utilizing transgenic mice where BDNF overexpression was controlled by the beta-actin promoter, we evaluated the effects of long-term overexpression of BDNF on the dendritic structure of granule cells in the hippocampal dentate gyrus. BDNF transgenic mice provided the opportunity to investigate the effects of modestly increased BDNF levels on dendrite structure in the complex in vivo environment. While the elevated BDNF levels were insufficient to change levels of TrkB receptor isoforms or downstream TrkB signaling, they did increase dendrite complexity of dentate granule cells. These cells showed an increased number of first order dendrites, of total dendritic length and of total number of branch points. These results suggest that dendrite structure of granule cells is tightly regulated and is sensitive to modest increases in levels of BDNF. This is the first study to evaluate the effects of BDNF overexpression on dendrite morphology in the intact hippocampus and extends previous in vitro observations that BDNF influences synaptic plasticity by increasing complexity of dendritic arbors. (C) 2002 IBRO Published by Elsevier Science Ltd. All rights reserved.
引用
收藏
页码:795 / 805
页数:11
相关论文
共 52 条
[1]  
ALLENDOERFER KL, 1994, J NEUROSCI, V14, P1795
[2]   The TrkB-Shc site signals neuronal survival and local axon growth via MEK and PI3-kinase [J].
Atwal, JK ;
Massie, B ;
Miller, FD ;
Kaplan, DR .
NEURON, 2000, 27 (02) :265-277
[3]   THE TRK FAMILY OF NEUROTROPHIN RECEPTORS [J].
BARBACID, M .
JOURNAL OF NEUROBIOLOGY, 1994, 25 (11) :1386-1403
[4]   In sympathetic but not sensory neurones, phosphoinositide-3 kinase is important for NGF-dependent survival and the retrograde transport of I-125-beta NGF [J].
Bartlett, SE ;
Reynolds, AJ ;
Weible, M ;
Heydon, K ;
Hendry, IA .
BRAIN RESEARCH, 1997, 761 (02) :257-262
[5]  
Baxter GT, 1997, J NEUROSCI, V17, P2683
[6]  
BIFFO S, 1995, DEVELOPMENT, V121, P2461
[7]   Rho GTPases and their effector proteins [J].
Bishop, AL ;
Hall, A .
BIOCHEMICAL JOURNAL, 2000, 348 (02) :241-255
[8]   CHARACTERIZATION OF NERVE GROWTH-FACTOR (NGF) RELEASE FROM HIPPOCAMPAL-NEURONS - EVIDENCE FOR A CONSTITUTIVE AND AN UNCONVENTIONAL SODIUM-DEPENDENT REGULATED PATHWAY [J].
BLOCHL, A ;
THOENEN, H .
EUROPEAN JOURNAL OF NEUROSCIENCE, 1995, 7 (06) :1220-1228
[9]  
Buckmaster PS, 2001, J COMP NEUROL, V430, P264, DOI 10.1002/1096-9861(20010205)430:2<264::AID-CNE1030>3.0.CO
[10]  
2-3