Mechanisms Underlying Changes in Encoding of Neuronal Information by Backward Travelling Action Potentials

Publication Date

4-6-2018

Document Type

Poster

Department

Biological Sciences

Mentor

Wolfgang Stein

Mentor Department

Biological Sciences

Abstract

Neurons encode stimuli by generating action potentials at the axon origin and propagating them along the axon trunk. However, axons can also possess secondary (ectopic) action potentials initiation sites, far from the stimulus encoding site, the axon origin. Action potentials initiated at ectopic sites travel both forward and backward along the axon. We have previously shown that when action potentials travel backward they change how stimuli are encoded in neurons using an experimentally advantageous neuron in the stomatogastric nervous system of the crab, Cancer borealis. Specifically, increases in the frequency of ectopic action potentials delay the start time of encoding, reduce the number of action potentials produced, and decrease the burst duration of the encoded stimuli. While backward travelling action potentials clearly affect encoding, the mechanism underlying their actions remains unclear. Our current computational modelling indicates that these changes to encoding require a slow hyperpolarizing current to be present at the site of encoding. However, what this current changes at the site of initiation to promote changes in encoding remains unclear. Preliminary results indicate that as this current accumulates with increasing ectopic action potential frequencies, the total membrane conductance increases and the membrane potential hyperpolarizes. Consequently, other voltage-gated ionic conductances at the site of encoding are also affected, i.e. their open probabilities and activation states change. We hypothesize that the changes in membrane potential alone are necessary and sufficient to elicit the observed ectopic action potential frequency dependent modulation of sensory encoding. We are currently testing this hypothesis using models, which allow us to alter the membrane potential at the site of encoding independent of ectopic action potential frequency. This will provide a better understanding of the underlying mechanism facilitating the effects backward travelling action potentials on encoding observed physiologically.

Comments

DeMaegd-graduate

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