Recombinant BDNF rescues deficits in basal synaptic transmission and hippocampal LTP in BDNF knockout mice

被引:1048
作者
Patterson, SL [1 ]
Abel, T [1 ]
Deuel, TAS [1 ]
MArtin, KC [1 ]
Rose, JC [1 ]
Kandel, ER [1 ]
机构
[1] COLUMBIA UNIV COLL PHYS & SURG, CTR NEUROBIOL & BEHAV, NEW YORK, NY 10032 USA
关键词
D O I
10.1016/S0896-6273(00)80140-3
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Brain-derived neurotrophic factor (BDNF) is expressed at high levels in hippocampal neurons, and its expression is modulated by neural activity. Knockout mice can be used to study the roles of molecules like BDNF in synaptic plasticity with more molecular specificity than is possible using pharmacological approaches. Because in conventional knockouts the disrupted gene product is absent in all tissues throughout the life of the animal, developmental effects may complicate the interpretation of deficits in the adult. Rescue experiments can help to distinguish between developmental and acute requirements for the missing gene product. We here demonstrate that treatment of hippocampal slices from BDNF knockout mice with recombinant BDNF completely reverses deficits in longterm potentiation and significantly improves deficits in basal synaptic transmission at the Schaffer collateral-CA1 synapse. Thus, BDNF has an acute role in hippocampal synaptic function.
引用
收藏
页码:1137 / 1145
页数:9
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