Engrailed Alters the Specificity of Synaptic Connections of Drosophila Auditory Neurons with the Giant Fiber
Engrailed Alters the Specificity of Synaptic Connections of Drosophila Auditory Neurons with the Giant Fiber
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DOI：
10.1523/jneurosci.1939-14.2014
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发表时间：
2014-08-27
影响因子：
5.3
通讯作者：
Blagburn, Jonathan M.
中科院分区：
文献类型：
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作者：
Pezier, Adeline;Jezzini, Sami H.;Blagburn, Jonathan M.
我们发现，一个子集的声音检测约翰斯顿的器官神经元（容斯）在果蝇，表达的转录因子Engrailed（En）和Invected（Inv），形成混合的电和化学突触输入到巨纤维（GF）树突。这些突触连接通过跨突触神经生物素（NB）转移和通过Bruchpilot-短点的共定位来检测。然后，我们表明，错误表达En有丝分裂后在第二个子集的声音响应容斯导致他们形成异位的电和化学突触的GF，反过来又导致突触后神经元重新分配到这些传入附近的树突状分支。我们还介绍了一个简单的电生理记录范例，用于量化突触前和突触后的电活动在这个突触，通过测量细胞外的声音诱发电位（SEP）从触角神经，同时监测的可能性的GF发射动作电位响应于同时阈下的声音和电压刺激。En的异位突触前表达加强了突触连接，这与形成更多的突触接触一致。最后，RNAi介导的有丝分裂后神经元中En和Inv的敲低降低了SEP振幅，但也降低了JON-GF突触处的突触强度。总的来说，这些结果表明，在容斯的En和Inv调节神经元的兴奋性和突触连接。
We show that a subset of sound-detecting Johnston's Organ neurons (JONs) in Drosophila melanogaster, which express the transcription factors Engrailed (En) and Invected (Inv), form mixed electrical and chemical synaptic inputs onto the giant fiber (GF) dendrite. These synaptic connections are detected by trans-synaptic Neurobiotin (NB) transfer and by colocalization of Bruchpilot-short puncta. We then show that misexpressing En postmitotically in a second subset of sound-responsive JONs causes them to form ectopic electrical and chemical synapses with the GF, in turn causing that postsynaptic neuron to redistribute its dendritic branches into the vicinity of these afferents. We also introduce a simple electrophysiological recording paradigm for quantifying the presynaptic and postsynaptic electrical activity at this synapse, by measuring the extracellular sound-evoked potentials (SEPs) from the antennal nerve while monitoring the likelihood of the GF firing an action potential in response to simultaneous subthreshold sound and voltage stimuli. Ectopic presynaptic expression of En strengthens the synaptic connection, consistent with there being more synaptic contacts formed. Finally, RNAi-mediated knockdown of En and Inv in postmitotic neurons reduces SEP amplitude but also reduces synaptic strength at the JON-GF synapse. Overall, these results suggest that En and Inv in JONs regulate both neuronal excitability and synaptic connectivity.