Secreted form of beta-amyloid precursor protein shifts the frequency dependency for induction of LTD, and enhances LTP in hippocampal slices

被引:156
作者
Ishida, A [1 ]
Furukawa, K [1 ]
Keller, JN [1 ]
Mattson, MP [1 ]
机构
[1] UNIV KENTUCKY,LEXINGTON,KY 40536
关键词
Alzheimer's disease; calcium; cyclic GMP; excitotoxicity; learning and memory; long-term potentiation; phosphorylation; synaptic plasticity;
D O I
10.1097/00001756-199707070-00009
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
THE secreted form of beta-amyloid precursor protein (sAPP alpha) is released from neurons in an activity-dependent manner, and has been reported to modulate neuronal excitability in dissociated hippocampal neurons. We now report that sAPP alpha shifts the frequency dependence for induction of long-term depression of synaptic transmission (LTD) in hippocampal slices from adult rats. Whereas low frequency stimulation (1 Hz) of Schaffer collateral axons induced LTD of the postsynaptic response of CA1 neurons in control slices, it did not induce LTD in slices pretreated with sAPP alpha. On the other hand, whereas a 10 Hz stimulation normally induced neither LTD or LTP, it did induce LTD in slices pretreated with sAPP alpha, sAPP alpha potentiated LTP induced by high frequency stimulation. sAPP alpha induced cGMP production in hippocampal slices, and pretreatment of slices with 8-bromo-cyclic GMP mimicked the effect of sAPP alpha on LTD suggesting a role for cyclic GMP in modulation of LTD. The data suggest an important role for sAPP alpha in modulation of synaptic plasticity in the hippocampus.
引用
收藏
页码:2133 / 2137
页数:5
相关论文
共 31 条
[1]   THE SECRETED FORM OF THE ALZHEIMERS BETA-AMYLOID PRECURSOR PROTEIN STIMULATES A MEMBRANE-ASSOCIATED GUANYLATE-CYCLASE [J].
BARGER, SW ;
MATTSON, MP .
BIOCHEMICAL JOURNAL, 1995, 311 :45-47
[2]  
Barger SW, 1996, MOL BRAIN RES, V40, P116
[3]  
BARGER SW, 1996, J NEUROCHEM, V40, P116
[4]  
Bear Mark F., 1994, Current Opinion in Neurobiology, V4, P389, DOI 10.1016/0959-4388(94)90101-5
[5]   MECHANISM FOR A SLIDING SYNAPTIC MODIFICATION THRESHOLD [J].
BEAR, MF .
NEURON, 1995, 15 (01) :1-4
[6]   NITRIC OXIDE-DEPENDENT LONG-TERM POTENTIATION IS BLOCKED BY A SPECIFIC INHIBITOR OF SOLUBLE GUANYLYL CYCLASE [J].
BOULTON, CL ;
SOUTHAM, E ;
GARTHWAITE, J .
NEUROSCIENCE, 1995, 69 (03) :699-703
[7]   THE NITRIC-OXIDE CYCLIC-GMP PATHWAY AND SYNAPTIC DEPRESSION IN RAT HIPPOCAMPAL SLICES [J].
BOULTON, CL ;
IRVING, AJ ;
SOUTHAM, E ;
POTIER, B ;
GARTHWAITE, J ;
COLLINGRIDGE, GL .
EUROPEAN JOURNAL OF NEUROSCIENCE, 1994, 6 (10) :1528-1535
[8]   RELEASE OF EXCESS AMYLOID BETA-PROTEIN FROM A MUTANT AMYLOID BETA-PROTEIN PRECURSOR [J].
CAI, XD ;
GOLDE, TE ;
YOUNKIN, SG .
SCIENCE, 1993, 259 (5094) :514-516
[9]   EXCESSIVE PRODUCTION OF AMYLOID BETA-PROTEIN BY PERIPHERAL CELLS OF SYMPTOMATIC AND PRESYMPTOMATIC PATIENTS CARRYING THE SWEDISH FAMILIAL ALZHEIMER-DISEASE MUTATION [J].
CITRON, M ;
VIGOPELFREY, C ;
TEPLOW, DB ;
MILLER, C ;
SCHENK, D ;
JOHNSTON, J ;
WINBLAD, B ;
VENIZELOS, N ;
LANNFELT, L ;
SELKOE, DJ .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1994, 91 (25) :11993-11997
[10]   INTRAVENTRICULAR INFUSIONS OF ANTIBODIES TO AMYLOID-BETA-PROTEIN PRECURSOR IMPAIR THE ACQUISITION OF A PASSIVE-AVOIDANCE RESPONSE IN THE RAT [J].
DOYLE, E ;
BRUCE, MT ;
BREEN, KC ;
SMITH, DC ;
ANDERTON, B ;
REGAN, CM .
NEUROSCIENCE LETTERS, 1990, 115 (01) :97-102