α钙/钙调蛋白依赖性蛋白激酶II的自磷酸化并非成年小鼠中NMDA受体依赖性长时程增强的普遍必要条件。
Autophosphorylation of alphaCaMKII is not a general requirement for NMDA receptor-dependent LTP in the adult mouse.
作者信息
Cooke Sam F, Wu Jianqun, Plattner Florian, Errington Michael, Rowan Michael, Peters Marco, Hirano Ayumi, Bradshaw Karl D, Anwyl Roger, Bliss Timothy V P, Giese K Peter
机构信息
MRC National Institute for Medical Research, Mill Hill, London NW7 1AA, UK.
出版信息
J Physiol. 2006 Aug 1;574(Pt 3):805-18. doi: 10.1113/jphysiol.2006.111559. Epub 2006 May 25.
Abstract
Autophosphorylation of alpha-Ca2+/calmodulin kinase II (alphaCaMKII) at Thr286 is thought to be a general effector mechanism for sustaining transcription-independent long-term potentiation (LTP) at pathways where LTP is NMDA receptor-dependent. We have compared LTP at two such hippocampal pathways in mutant mice with a disabling point mutation at the Thr286 autophosphorylation site. We find that autophosphorylation of alphaCaMKII is essential for induction of LTP at Schaffer commissural-CA1 synapses in vivo, but is not required for LTP that can be sustained over days at medial perforant path-granule cell synapses in awake mice. At these latter synapses LTP is supported by cyclic AMP-dependent signalling in the absence of alphaCaMKII signalling. Thus, the autophosphorylation of alphaCaMKII is not a general requirement for NMDA receptor-dependent LTP in the adult mouse.
摘要
α-Ca²⁺/钙调蛋白激酶II（αCaMKII）在苏氨酸286位点的自磷酸化被认为是在长时程增强（LTP）依赖N-甲基-D-天冬氨酸（NMDA）受体的通路中维持转录非依赖性长时程增强的一种普遍效应机制。我们比较了在苏氨酸286自磷酸化位点存在失活性点突变的突变小鼠中两条此类海马通路的长时程增强。我们发现，αCaMKII的自磷酸化对于体内诱导海马联合-海马脑区1（Schaffer commissural-CA1）突触的长时程增强至关重要，但对于清醒小鼠内侧穿通通路-颗粒细胞突触中可持续数天的长时程增强则不是必需的。在这些后者的突触中，在没有αCaMKII信号传导的情况下，长时程增强由环磷酸腺苷（cAMP）依赖性信号传导支持。因此，αCaMKII的自磷酸化并非成年小鼠中NMDA受体依赖性长时程增强的普遍要求。
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