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Rapid BDNF-induced retrograde synaptic modification in a developing retinotectal system

机译：快速的BDNF诱导的视网膜-视网膜系统中逆行突触修饰。

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摘要

In cultures of hippocampal neurons, induction of long-term synaptic potentiation or depression by repetitive synaptic activity is accompanied by a retrograde spread of potentiation or depression, respectively, from the site of induction at the axonal outputs to the input synapses on the dendrites of the presynaptic neuron(1,2). We report here that rapid retrograde synaptic modification also exists in an intact developing retinotectal system. Local application of brain-derived neurotrophic factor ( BDNF) to the Xenopus laevis optic tectum, which induced persistent potentiation of retinotectal synapses, led to a rapid modification of synaptic inputs at the dendrites of retinal ganglion cells (RGCs), as shown by a persistent enhancement of light-evoked excitatory synaptic currents and spiking activity of RGCs. This retrograde effect required TrkB receptor activation, phospholipase Cgamma activity and Ca2+ elevation in RGCs, and was accounted for by a selective increase in the number of postsynaptic AMPA-subtype glutamate receptors at RGC dendrites. Such retrograde information flow in the neuron allows rapid regulation of synaptic inputs at the dendrite in accordance to signals received at axon terminals, a process reminiscent of back-propagation algorithm for learning in neural networks(3).
机译：在海马神经元的培养物中，通过反复的突触活性诱导长期突触增强或抑制伴随着增强或抑制的逆行扩散，分别从轴突输出的诱导位点到突触的树突上的输入突触。突触前神经元（1,2）。我们在这里报告，快速逆行的突触修饰也存在于完整的发育中的视网膜-皮层系统中。脑源性神经营养因子（BDNF）在非洲爪蟾视神经覆盖物上的局部应用可诱导视网膜-视神经突触的持续增强，从而导致视网膜神经节细胞（RGC）的树突中突触输入的快速修饰，如持续存在增强光诱发的兴奋性突触电流和RGC的突波活性。这种逆行作用需要RGC中的TrkB受体活化，磷脂酶Cgamma活性和Ca2 +升高，并且是由于RGC树突中突触后AMPA亚型谷氨酸受体数量的选择性增加而引起的。神经元中的这种逆行信息流可以根据轴突末端接收到的信号快速调节树突状突触的输入，这一过程让人想起在神经网络中学习的反向传播算法（3）。

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