科研之友
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摘要
Non-technical summary @@@ Information is coded in the form of bursts of electrical impulses propagating among nerve cells which form complex networks in the brain. Effective communication between these cells depends on the ability for cross-talk among them through release and reception of chemical substances (neurotransmitters). This study uses the hearing system as a model to show that the patterns of electrical impulses can dramatically impact the amount of neurotransmitter released. When presented in short clusters, these impulses are more effective in releasing neurotransmitters than those composed of the same number of impulses but given continuously. Our findings may potentially help us understand how nerve cells code and transfer information in the mammalian brain, and in particular, how auditory neurons localize the sound source in space.Patterns of action potentials (APs), often in the form of bursts, are critical for coding and processing information in the brain. However, how AP bursts modulate secretion at synapses remains elusive. Here, using the calyx of Held synapse as a model we compared synaptic release evoked by AP patterns with a different number of bursts while the total number of APs and frequency were fixed. The ratio of total release produced by multiple bursts to that by a single burst was defined as 'burst-effect'. We found that four bursts of 25 stimuli at 100 Hz increased the total charge of EPSCs to 1.47 +/- 0.04 times that by a single burst of 100 stimuli at the same frequency. Blocking AMPA receptor desensitization and saturation did not alter the burst-effect, indicating that it was mainly determined by presynaptic mechanisms. Simultaneous dual recordings of presynaptic membrane capacitance (C-m) and EPSCs revealed a similar burst-effect, being 1.58 +/- 0.13 by C-m and 1.49 +/- 0.05 by EPSCs. Reducing presynaptic Ca2+ influx by lowering extracellular Ca2+ concentration or buffering residual intracellular Ca2+ with EGTA inhibited the burst-effect. We further developed a computational model largely recapitulating the burst-effect and demonstrated that this effect is highly sensitive to dynamic change in availability of the releasable pool of synaptic vesicles during various patterns of activities. Taken together, we conclude that AP bursts modulate synaptic output mainly through intricate interaction between depletion and replenishment of the large releasable pool. This burst-effect differs from the somatic burst-effect previously described from adrenal chromaffin cells, which substantially depends on activity-induced accumulation of Ca2+ to facilitate release of a limited number of vesicles in the releasable pool. Hence, AP bursts may play an important role in dynamically regulating synaptic strength and fidelity during intense neuronal activity at central synapses.
