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Conditional spike backpropagation generates burst discharge in a sensory neuron
1Department of Cell Biology and Anatomy, Neuroscience Research Group, University of Calgary, Calgary, Alberta T2N 4N1, Canada.
Journal of Neurophysiology
|September 9, 2000
Summary
Repetitive neuronal firing causes a depolarizing shift in spike afterpotentials, leading to burst discharge. This shift is driven by dendritic sodium spikes, with burst termination linked to dendritic refractory periods.
Area of Science:
- Neuroscience
- Computational Neuroscience
Background:
- Pyramidal cells in the electrosensory lateral line lobe (ELL) exhibit burst firing patterns.
- Backpropagating dendritic spikes generate depolarizing afterpotentials (DAPs) at the soma.
- Repetitive firing leads to a depolarizing shift, triggering spike doublets and burst afterhyperpolarization (bAHP).
Purpose of the Study:
- Investigate soma-dendritic mechanisms controlling the depolarizing shift in somatic spike afterpotentials.
- Elucidate the mechanism by which spike doublets terminate spike discharge.
Main Methods:
- Intracellular recordings from ELL pyramidal somata and apical dendrites in an in vitro slice preparation.
- Used tetrodotoxin (TTX) to block backpropagating spikes and assess somatic afterpotential stability.
Main Results:
- Depolarizing shift is attributed to DAP amplitude potentiation, caused by frequency-dependent broadening and temporal summation of dendritic Na(+) spikes.
- Spike doublets occur when interspike intervals approach the somatic refractory period but fall within the dendritic refractory period.
- Burst termination is linked to the dendritic refractory period preventing backpropagation, allowing bAHP to hyperpolarize the membrane.
Conclusions:
- The transition from tonic to burst discharge depends on spike history and frequency, influencing dendritic spike invasion.
- Backpropagating spikes provide an intrinsic mechanism for generating rhythmic burst outputs in ELL pyramidal cells.