A tropomyosin-related kinase B ligand is required for ERK activation, long-term synaptic facilitation, and long-term memory in Aplysia
A tropomyosin-related kinase B ligand is required for ERK activation, long-term synaptic facilitation, and long-term memory in Aplysia
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DOI：
10.1073/pnas.0603412103
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发表时间：
2006-09-19
影响因子：
11.1
通讯作者：
Carew, Thomas J.
中科院分区：
文献类型：
--
作者：
Sharma, Shiv K.;Sherff, Carolyn M.;Carew, Thomas J.
BDNF在哺乳动物发育过程中通过原肌球蛋白相关激酶B（Trk B）受体发挥作用，也可增强成年失智症的长时程突触易化（LTF）。由于LTF是在失智症的长期记忆（LTM）的基板，我们检查了在LTM形成的分泌的TrkB配体的要求在分子，突触和行为水平。使用细胞外的融合蛋白，螯合分泌的TrkB配体，我们表明，TrkB功能所需的阿托宁诱导的细胞外信号调节激酶的激活，尾神经休克诱导的LTF在中枢神经系统中，和尾休克诱导的LTM，但不是必要的短期突触促进或短期记忆。这些结果表明，分泌的生长因子，通过TrkB信号级联反应，是诱导持久的可塑性和记忆形成的失智症的关键。
BDNF, which acts through tropomyosin-related kinase B (TrkB) receptors during mammalian development, also enhances long-term synaptic facilitation (LTF) in adult Aplysia. Because LTF is a substrate for long-term memory (LTM) in Aplysia, we examined the requirement of a secreted TrkB ligand in LTM formation at molecular, synaptic, and behavioral levels. Using an extracellular fusion protein that sequesters secreted TrkB ligands, we show that TrkB function is required for serotonin-induced activation of extracellular signal-regulated kinase, tail nerve shock-induced LTF in the CNS, and tail shock-induced LTM but is not necessary for short-term synaptic facilitation or short-term memory. These results show that a secreted growth factor, acting through a TrkB signaling cascade, is critical for the induction of long-lasting plasticity and memory formation in Aplysia.