Motoneurons can count: A cell intrinsic spike number memory compensates for deviations from rate coding
Huthmacher, L.; Hilgert, S.; Reichert, S.; Hürkey, S.; Ryglewski, S.; Duch, C.
Show abstract
Firing rate is an important means of encoding information in many types of neurons. A prime example is asynchronous flight as used by [~]600,000 insect species (Dudley, 2018), where wingbeat frequency and flight power output are controlled by a rate code of the flight power motoneurons (Hurkey et al., 2023). The five motoneurons that innervate the wing depressor muscle fibers translate different magnitudes of excitatory drive smoothly into changes of their common firing rates, which in turn, are linearly related to wing power output (Gordon and Dickinson, 2006). Such motoneuron input/output properties are called type-I excitability and are achieved by the expression of specific combinations of ion currents that linearize the frequency-input current curve. But are there additional motoneuron properties that compensate for acute perturbation of their rate code? Here we combine in vivo electrophysiology with Drosophila genetics to test for mechanisms that compensate for transient perturbation of rate coding during behavior. We show that MN intrinsic properties compensate for the occurrence of extra spikes by delaying the subsequent spikes, thus restoring rate coding fidelity. The underlying mechanism is dose and phase dependent. First, compensatory increases of subsequent interspike interval durations grow with the number of supernumerous spikes that interfere with coding. Second, the magnitude of the compensation for single extra spikes depends on when during an interspike interval these occur. This mechanism depends at least in part on axonally localized HCN channels and increases the fidelity of motoneuron rate coding in the light of perturbation during flight motor behavior.
Matching journals
The top 3 journals account for 50% of the predicted probability mass.
Similar papers in this journal
Similar papers in this journal
- Structural and functional synaptic plasticity induced by convergent synapse loss requires co-innervation in the Drosophila neuromuscular circuit 97%
- State-dependent modulation of activity in distinct layer 6 corticothalamic neurons in barrel cortex of awake mice 96%
- Excitation and inhibition delays within a feedforward inhibitory pathway modulate cerebellar Purkinje cell output in mice 95%
Similar papers in this journal
"Similar papers" are the closest papers from that journal in the model's embedding space. They show what the match is built on, but the ranking comes mostly from a classifier over the whole training set, not from these examples alone.