A juvenile form of postsynaptic hippocampal long-term potentiation in mice deficient for the AMPA receptor subunit GluR-A

被引:101
作者
Jensen, V
Kaiser, KMM
Borchardt, T
Adelmann, G
Rozov, A
Burnashev, N
Brix, C
Frotscher, M
Andersen, P
Hvalby, O
Sakmann, B
Seeburg, PH
Sprengel, R
机构
[1] Max Planck Inst Med Res, Dept Mol Neurobiol, D-69120 Heidelberg, Germany
[2] Univ Oslo, Inst Basic Med Sci, Dept Physiol, N-0317 Oslo, Norway
[3] Max Planck Inst Med Res, Dept Cell Physiol, D-69120 Heidelberg, Germany
[4] Univ Freiburg, Inst Anat, D-79104 Freiburg, Germany
来源
JOURNAL OF PHYSIOLOGY-LONDON | 2003年 / 553卷 / 03期
关键词
D O I
10.1113/jphysiol.2003.053637
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
In adult mice, long-term potentiation (LTP) of synaptic transmission at CA3-to-CA1 synapses induced by tetanic stimulation requires L-alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionate (AMPA) receptors containing GluR-A subunits. Here, we report a GluR-A-independent form of LTP, which is comparable in size to LTP in wild-type mice at postnatal day 14 (P14) but diminishes between P14 and P42 in brain slices of GluR-A-deficient mice. The GluR-A-independent form of LTP is sensitive to D(-)-2-amino-5-phosphonopentanoic acid (D-AP5), but lacks short-term potentiation (STP) and can also be observed in the pairing induction protocol. As judged by unaltered paired-pulse facilitation, this LTP form is postsynaptically expressed despite depleted extrasynaptic AMPA receptor pools with reduced levels of GluR-B, which accumulates in somata and synapses of CA1 pyramidal neurons in GluR-A-deficient mice. Our results show that in the developing hippocampus synaptic plasticity can be expressed by AMPA receptors lacking the GluR-A subunit.
引用
收藏
页码:843 / 856
页数:14
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