Courant Institute of Mathematical Sciences, New York University, New York, New York, United States of America.
PLoS Comput Biol. 2012;8(8):e1002622. doi: 10.1371/journal.pcbi.1002622. Epub 2012 Aug 23.
Several experiments indicate that there exists substantial synaptic-depression at the synapses between olfactory receptor neurons (ORNs) and neurons within the drosophila antenna lobe (AL). This synaptic-depression may be partly caused by vesicle-depletion, and partly caused by presynaptic-inhibition due to the activity of inhibitory local neurons within the AL. While it has been proposed that this synaptic-depression contributes to the nonlinear relationship between ORN and projection neuron (PN) firing-rates, the precise functional role of synaptic-depression at the ORN synapses is not yet fully understood. In this paper we propose two hypotheses linking the information-coding properties of the fly AL with the network mechanisms responsible for ORN-->AL synaptic-depression. Our first hypothesis is related to variance coding of ORN firing-rate information--once stimulation to the ORNs is sufficiently high to saturate glomerular responses, further stimulation of the ORNs increases the regularity of PN spiking activity while maintaining PN firing-rates. The second hypothesis proposes a tradeoff between spike-time reliability and coding-capacity governed by the relative contribution of vesicle-depletion and presynaptic-inhibition to ORN-->AL synaptic-depression. Synaptic-depression caused primarily by vesicle-depletion will give rise to a very reliable system, whereas an equivalent amount of synaptic-depression caused primarily by presynaptic-inhibition will give rise to a less reliable system that is more sensitive to small shifts in odor stimulation. These two hypotheses are substantiated by several small analyzable toy models of the fly AL, as well as a more physiologically realistic large-scale computational model of the fly AL involving 5 glomerular channels.
几项实验表明，在果蝇触角叶（AL）内的嗅觉受体神经元（ORN）和神经元之间存在大量的突触抑制。这种突触抑制可能部分是由囊泡耗竭引起的，部分是由 AL 内抑制性局部神经元的活动引起的突触前抑制引起的。虽然已经提出这种突触抑制有助于 ORN 和投射神经元（PN）放电率之间的非线性关系，但 ORN 突触抑制的确切功能作用尚未完全理解。在本文中，我们提出了两个假设，将果蝇 AL 的信息编码特性与负责 ORN- > AL 突触抑制的网络机制联系起来。我们的第一个假设与 ORN 放电率信息的方差编码有关——一旦 ORN 的刺激足够高以使肾小球反应饱和，进一步刺激 ORN 会增加 PN 尖峰活动的规律性，同时保持 PN 放电率。第二个假设提出了由囊泡耗竭和突触前抑制对 ORN- > AL 突触抑制的相对贡献决定的尖峰时间可靠性和编码容量之间的权衡。主要由囊泡耗竭引起的突触抑制将产生一个非常可靠的系统，而由突触前抑制引起的同等数量的突触抑制将产生一个不太可靠的系统，对气味刺激的微小变化更敏感。这两个假设得到了几个小型的果蝇 AL 可分析玩具模型以及涉及 5 个肾小球通道的更生理现实的果蝇 AL 大规模计算模型的支持。
