Department of Neurology, Duke University School of Medicine , Durham, North Carolina.
Department of Neurobiology, Duke University School of Medicine , Durham, North Carolina.
J Neurophysiol. 2019 Feb 1;121(2):609-619. doi: 10.1152/jn.00669.2018. Epub 2018 Dec 5.
Hippocampal mossy fiber axons simultaneously activate CA3 pyramidal cells and stratum lucidum interneurons (SLINs), the latter providing feedforward inhibition to control CA3 pyramidal cell excitability. Filopodial extensions of giant boutons of mossy fibers provide excitatory synaptic input to the SLIN. These filopodia undergo extraordinary structural plasticity causally linked to execution of memory tasks, leading us to seek the mechanisms by which activity regulates these synapses. High-frequency stimulation of the mossy fibers induces long-term depression (LTD) of their calcium-permeable AMPA receptor synapses with SLINs; previous work localized the site of induction to be postsynaptic and the site of expression to be presynaptic. Yet, the underlying signaling events and the identity of the retrograde signal are incompletely understood. We used whole cell recordings of SLINs in hippocampal slices from wild-type and mutant mice to explore the mechanisms. Genetic and pharmacologic perturbations revealed a requirement for both the receptor tyrosine kinase TrkB and its agonist, brain-derived neurotrophic factor (BDNF), for induction of LTD. Inclusion of inhibitors of Trk receptor kinase and PLC in the patch pipette prevented LTD. Endocannabinoid receptor antagonists and genetic deletion of the CB1 receptor prevented LTD. We propose a model whereby release of BDNF from mossy fiber filopodia activates TrkB and PLCγ1 signaling postsynaptically within SLINs, triggering synthesis and release of an endocannabinoid that serves as a retrograde signal, culminating in reduced glutamate release. Insights into the signaling pathways by which activity modifies function of these synapses will facilitate an understanding of their contribution to the local circuit and behavioral consequences of hippocampal granule cell activity. NEW & NOTEWORTHY We investigated signaling mechanisms underlying plasticity of the hippocampal mossy fiber filopodial synapse with interneurons in stratum lucidum. High-frequency stimulation of the mossy fibers induces long-term depression of this synapse. Our findings are consistent with a model in which brain-derived neurotrophic factor released from filopodia activates TrkB of a stratum lucidum interneuron; the ensuing activation of PLCγ1 induces synthesis of an endocannabinoid, which provides a retrograde signal leading to reduced release of glutamate presynaptically.
海马来复纤维轴突同时激活 CA3 锥体神经元和层状亮区中间神经元(SLIN),后者提供前馈抑制以控制 CA3 锥体神经元的兴奋性。海马来复纤维的巨末梢的丝状伪足提供兴奋性突触输入到 SLIN。这些丝状伪足经历非凡的结构可塑性,与执行记忆任务因果相关,这促使我们寻求活动调节这些突触的机制。海马来复纤维的高频刺激诱导其与 SLIN 的钙通透性 AMPA 受体突触的长时程抑制(LTD);先前的工作将诱导部位定位在突触后,表达部位定位在突触前。然而,潜在的信号事件和逆行信号的身份仍不完全清楚。我们使用来自野生型和突变小鼠海马切片中 SLIN 的全细胞膜片钳记录来探索这些机制。遗传和药理学扰动表明,受体酪氨酸激酶 TrkB 及其激动剂脑源性神经营养因子(BDNF)对于 LTD 的诱导都是必需的。在膜片钳中包含 Trk 受体激酶和 PLC 的抑制剂可防止 LTD。内源性大麻素受体拮抗剂和 CB1 受体的基因缺失可防止 LTD。我们提出了一个模型,即来自海马来复纤维丝状伪足的 BDNF 的释放激活 SLIN 内的 TrkB 和 PLCγ1 信号转导,触发内源性大麻素的合成和释放,作为逆行信号,最终导致谷氨酸释放减少。深入了解活动改变这些突触功能的信号通路将有助于理解它们对海马颗粒细胞活动的局部回路和行为后果的贡献。新的和值得注意的是,我们研究了海马苔藓纤维丝状伪足突触与层状亮区中间神经元可塑性的信号转导机制。海马来复纤维的高频刺激诱导该突触的 LTD。我们的发现与以下模型一致:来自丝状伪足的脑源性神经营养因子激活 SLIN 中间神经元的 TrkB;随后 PLCγ1 的激活诱导内源性大麻素的合成,该内源性大麻素提供逆行信号,导致突触前谷氨酸释放减少。