Differential regulation of p75 and trkB mRNA expression after depolarizing stimuli or BDNF treatment in basal forebrain neuron cultures

被引:10
作者
Elliott, RC [1 ]
Black, IB [1 ]
Dreyfus, CF [1 ]
机构
[1] Univ Med & Dent New Jersey, Robert Wood Johnson Med Sch, Dept Neurosci & Cell Biol, Piscataway, NJ 08854 USA
关键词
neurotrophin; receptor; hippocampus; plasticity; activity;
D O I
10.1002/jnr.1199
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Extensive evidence suggests that BDNF regulates neural function and architecture after depolarization. Expression of BDNF is increased after depolarization, and the ability of BDNF to modulate synaptic function is well documented. To further investigate BDNF signaling after activity, we analyzed the effects of depolarization or BDNF treatment on receptor mRNA expression in cultured basal forebrain neurons. Levels of mRNA coding for the cognate BDNF receptor, trkB, as well as the common neurotrophin receptor, p75, were quantitated simultaneously using a sensitive solution hybridization technique. Depolarization or BDNF treatment increased p75 mRNA expression 94% and 195%, respectively. In contrast, trkB message decreased 23% after depolarization but was unchanged by BDNF treatment. Together, these changes resulted in significant increases in the p75/trkB ratio after depolarization or BDNF treatment that could alter BDNF binding or signal transduction. (C) 2001 Wiley-Liss, Inc.
引用
收藏
页码:83 / 88
页数:6
相关论文
共 54 条
[1]   BRAIN-DERIVED NEUROTROPHIC FACTOR INCREASES SURVIVAL AND DIFFERENTIATED FUNCTIONS OF RAT SEPTAL CHOLINERGIC NEURONS IN CULTURE [J].
ALDERSON, RF ;
ALTERMAN, AL ;
BARDE, YA ;
LINDSAY, RM .
NEURON, 1990, 5 (03) :297-306
[2]   The p75 neurotrophin receptor mediates neuronal apoptosis and is essential for naturally occurring sympathetic neuron death [J].
Bamji, SX ;
Majdan, M ;
Pozniak, CD ;
Belliveau, DJ ;
Aloyz, R ;
Kohn, J ;
Causing, CG ;
Miller, FD .
JOURNAL OF CELL BIOLOGY, 1998, 140 (04) :911-923
[3]  
Barde YA, 1987, PROG BRAIN RES <D>, V71, P185
[4]   DISRUPTION OF NGF BINDING TO THE LOW-AFFINITY NEUROTROPHIN RECEPTOR P75(LNTR) REDUCES NGF BINDING TO TRKA ON PC12 CELLS [J].
BARKER, PA ;
SHOOTER, EM .
NEURON, 1994, 13 (01) :203-215
[5]   DIFFERENTIAL EXPRESSION OF NERVE GROWTH-FACTOR RECEPTORS LEADS TO ALTERED BINDING-AFFINITY AND NEUROTROPHIN RESPONSIVENESS [J].
BENEDETTI, M ;
LEVI, A ;
CHAO, MV .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1993, 90 (16) :7859-7863
[6]   REGULATION OF NEUROTROPHIN AND TRKA, TRKB AND TRKC TYROSINE KINASE RECEPTOR MESSENGER-RNA EXPRESSION IN KINDLING [J].
BENGZON, J ;
KOKAIA, Z ;
ERNFORS, P ;
KOKAIA, M ;
LEANZA, G ;
NILSSON, OG ;
PERSSON, H ;
LINDVALL, O .
NEUROSCIENCE, 1993, 53 (02) :433-446
[7]   GROWTH OF A RAT NEUROBLASTOMA CELL LINE IN SERUM-FREE SUPPLEMENTED MEDIUM [J].
BOTTENSTEIN, JE ;
SATO, GH .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1979, 76 (01) :514-517
[8]   GENE-TRANSFER AND MOLECULAR-CLONING OF THE HUMAN NGF RECEPTOR [J].
CHAO, MV ;
BOTHWELL, MA ;
ROSS, AH ;
KOPROWSKI, H ;
LANAHAN, AA ;
BUCK, CR ;
SEHGAL, A .
SCIENCE, 1986, 232 (4749) :518-521
[9]   NEUROTROPHIN RECEPTORS - A WINDOW INTO NEURONAL DIFFERENTIATION [J].
CHAO, MV .
NEURON, 1992, 9 (04) :583-593
[10]   ISOLATION OF BIOLOGICALLY-ACTIVE RIBONUCLEIC-ACID FROM SOURCES ENRICHED IN RIBONUCLEASE [J].
CHIRGWIN, JM ;
PRZYBYLA, AE ;
MACDONALD, RJ ;
RUTTER, WJ .
BIOCHEMISTRY, 1979, 18 (24) :5294-5299