MAP kinase translocates into the nucleus of the presynaptic cell and is required for long-term facilitation in Aplysia
MAP kinase translocates into the nucleus of the presynaptic cell and is required for long-term facilitation in Aplysia
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DOI：
10.1016/s0896-6273(00)80330-x
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发表时间：
1997-06-01
期刊：
影响因子：
16.2
通讯作者：
Kandel, ER
中科院分区：
文献类型：
--
作者：
Martin, KC;Michael, D;Kandel, ER
在失智症中感觉到运动突触的长期促进需要基因表达。虽然一些参与长期易化的转录因子被PKA磷酸化，但其他转录因子缺乏PKA位点，但含有MAP激酶（MAPK）磷酸化位点。我们现在表明，MAPK易位到突触前的细胞核，但不是突触后细胞在5-HT诱导的长期促进。MAPK的突触前核转位也由细胞内cAMP的升高触发。将抗MAPK抗体或MAPK激酶抑制剂注射到突触前细胞中阻断长时程易化，而不影响基础突触传递或短时程易化。因此，MAPK似乎是专门招募和必要的长期形式的促进。这种长时程可塑性的机制可能是相当普遍的：cAMP也激活了小鼠海马神经元中的MAPK，这表明MAPK可能在海马长时程增强中发挥作用。
Long-term facilitation of the sensory to motor synapse in Aplysia requires gene expression. While some transcription factors involved in long-term facilitation are phosphorylated by PKA, others lack PKA sites but contain MAP Kinase (MAPK) phosphorylation sites. We now show that MAPK translocates into the nucleus of the presynaptic but not the postsynaptic cell during 5-HT-induced long-term facilitation. The presynaptic nuclear translocation of MAPK is also triggered by elevations in intracellular cAMP. Injection of anti-MAPK antibodies or of MAPK Kinase inhibitors into the presynaptic cell blocks long-term facilitation, without affecting basal synaptic transmission or short-term facilitation. Thus, MAPK appears to be specifically recruited and necessary for the long-term form of facilitation. This mechanism for long-term plasticity may be quite general: cAMP also activated MAPK in mouse hippocampal neurons, suggesting that MAPK may play a role in hippocampal long-term potentiation.