The actions of BDNF on dendritic spine density and morphology in organotypic slice cultures depend on the presence of serum in culture media

被引:60
作者
Chapleau, Christopher A. [1 ]
Carlo, Maria E. [1 ]
Larimore, Jennifer L. [1 ]
Pozzo-Miller, Lucas [1 ]
机构
[1] Univ Alabama Birmingham, Dept Neurobiol, Civitan Int Res Ctr, McKnight Brain Inst, Birmingham, AL 35294 USA
关键词
CAI pyramidal neuron; biolistic transfection; hippocampus; confocal microscopy; enhanced yellow fluorescent protein; organotypic slice culture;
D O I
10.1016/j.jneumeth.2007.12.006
中图分类号
Q5 [生物化学];
学科分类号
071010 ; 081704 ;
摘要
We have previously shown that brain-derived neurotrophin factor (BDNF) increases dendritic spine density and the proportion of stubby spines in apical dendrites of CAI pyramidal neurons of hippocampal slice cultures maintained in serum-free media. We show here that serum withdrawal causes an increase in the proportion of thin spines and a decrease in the fraction of stubby spines, without changing the overall density of dendritic spines. When slices are maintained in serum-containing media, BDNF also increased spine density but had the opposite effect on spine morphology: it increased the proportion of mushroom and thin spines and decreased the proportion of stubby spines. Intriguingly, slices maintained in serum media showed a lower p75NTR-to-TrkB expression level than serum-free slices, even after BDNF exposure. The differential actions of BDNF on spine morphology depending on the presence of serum in culture media, together with the difference in neurotrophin receptor expression are reminiscent of opposing functional signaling by p75NTR and Trk receptors, and reveal a complex modulation of dendritic morphology by BDNF signaling. (c) 2008 Elsevier B.V. All rights reserved.
引用
收藏
页码:182 / 190
页数:9
相关论文
共 66 条
[1]   Induction of long-term potentiation and depression is reflected by corresponding changes in secretion of endogenous brain-derived neurotrophic factor [J].
Aicardi, G ;
Argilli, E ;
Cappello, S ;
Santi, S ;
Riccio, M ;
Thoenen, H ;
Canossa, M .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2004, 101 (44) :15788-15792
[2]   ERK1/2 activation is necessary for BDNF to increase dendritic spine density in hippocampal CA1 pyramidal neurons [J].
Alonso, M ;
Medina, JH ;
Pozzo-Miller, L .
LEARNING & MEMORY, 2004, 11 (02) :172-178
[3]  
Amaral MD, 2005, SYNAPTIC PLASTICITY AND TRANSSYNAPTIC SIGNALING, P185, DOI 10.1007/0-387-25443-9_12
[4]   BDNF induces calcium elevations associated with IBDNF, a nonselective cationic current mediated by TRPC channels [J].
Amaral, Michelle D. ;
Pozzo-Miller, Lucas .
JOURNAL OF NEUROPHYSIOLOGY, 2007, 98 (04) :2476-2482
[5]   TRPC3 channels are necessary for brain-derived neurotrophic factor to activate a nonselective cationic current and to induce dendritic spine formation [J].
Amaral, Michelle D. ;
Pozzo-Miller, Lucas .
JOURNAL OF NEUROSCIENCE, 2007, 27 (19) :5179-5189
[6]   Transient receptor potential channels as novel effectors of brain-derived neurotrophic factor signaling: Potential implications for Rett syndrome [J].
Amaral, Michelle D. ;
Chapleau, Christopher A. ;
Pozzo-Miller, Lucas .
PHARMACOLOGY & THERAPEUTICS, 2007, 113 (02) :394-409
[7]  
Balkowiec A, 2002, J NEUROSCI, V22, P10399
[8]  
BARBACID M, 1993, ONCOGENE, V8, P2033
[9]  
Black IB, 1999, J NEUROBIOL, V41, P108, DOI 10.1002/(SICI)1097-4695(199910)41:1<108::AID-NEU14>3.0.CO
[10]  
2-U