![]() ![]() Here, we propose that spikelets occur when an AP initiated at the axon initial segment only propagates down the axon, but fails to activate sodium currents in the soma and dendrites. However, besides APs, pyramidal cells sometimes also show somatic spikelets-small depolarizations with an AP-like shape-whose origin remains unclear. Concurrently, the AP also propagates back to the soma and into the dendrites where it might trigger synaptic plasticity, which is the basis of learning and memory. According to textbook knowledge, an AP in pyramidal neurons is initiated at the axon initial segment and propagates along the axon to the next cell. ![]() Here we focus on pyramidal cells, which are the principal neurons in neocortex and hippocampus. Therefore, APs are the basis of neural function, yet some of their fundamental features are still not well understood. Because spikelets involve forward propagation of action potentials along the axon while they avoid full depolarization of the somato-dendritic compartments, we conjecture that this mode of operation saves energy and regulates dendritic plasticity while still allowing for a read-out of results of neuronal computations.Īction potentials (APs) are digital, all-or-none signals by which neurons communicate with each other. Using mathematical analysis and numerical simulations of compartmental neuron models, we identified four key factors controlling spikelet generation: (1) difference in firing threshold, (2) impedance mismatch, and (3) electrotonic separation between the soma and the axon initial segment, as well as (4) input amplitude. To explain spikelet generation, we propose a novel single-cell mechanism: somato-dendritic input generates action potentials at the axon initial segment that may fail to activate the soma and manifest as somatic spikelets. Their origin in pyramidal neurons remains controversial. Spikelets are small spike-like depolarizations that can be measured in somatic intracellular recordings.
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