Biomedical subjects

Liza Noonan

Publications and source records attributed to Liza Noonan.

3 recordsLinked to original sources

PubMed2003

A dynamic dendritic refractory period regulates burst discharge in the electrosensory lobe of weakly electric fish.

Na+-dependent spikes initiate in the soma or axon hillock region and actively backpropagate into the dendritic arbor of many central neurons. Inward currents underlying spike discharge are offset by outward K+ currents that repolarize a spike and establish a refractory period to temporarily prevent spike discharge. We show in a sensory neuron that somatic and dendritic K+ channels differentially control burst discharge by regulating the extent to which backpropagating dendritic spikes can re-excite the soma. During repetitive discharge a progressive broadening of dendritic spikes promotes a dynamic increase in dendritic spike refractory period. A leaky integrate-and-fire model shows that spike bursts are terminated when a decreasing somatic interspike interval and an increasing dendritic spike refractory period synergistically act to block backpropagation. The time required for the somatic interspike interval to intersect with dendritic refractory period determines burst frequency, a time that is regulated by somatic and dendritic spike repolarization. Thus, K+ channels involved in spike repolarization can efficiently control the pattern of spike output by establishing a soma-dendritic interaction that invokes dynamic shifts in dendritic spike properties.

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PubMed2003

Persistent Na+ current modifies burst discharge by regulating conditional backpropagation of dendritic spikes.

The estimation and detection of stimuli by sensory neurons is affected by factors that govern a transition from tonic to burst mode and the frequency characteristics of burst output. Pyramidal cells in the electrosensory lobe of weakly electric fish generate spike bursts for the purpose of stimulus detection. Spike bursts are generated during repetitive discharge when a frequency-dependent broadening of dendritic spikes increases current flow from dendrite to soma to potentiate a somatic depolarizing afterpotential (DAP). The DAP eventually triggers a somatic spike doublet with an interspike interval that falls inside the dendritic refractory period, blocking spike backpropagiation and the DAP. Repetition of this process gives rise to a rhythmic dendritic spike failure, termed conditional backpropagation, that converts cell output from tonic to burst discharge. Through in vitro recordings and compartmental modeling we show that burst frequency is regulated by the rate of DAP potentiation during a burst, which determines the time required to discharge the spike doublet that blocks backpropagation. DAP potentiation is magnified through a positive feedback process when an increase in dendritic spike duration activates persistent sodium current (I(NaP)). I(NaP) further promotes a slow depolarization that induces a shift from tonic to burst discharge over time. The results are consistent with a dynamical systems analysis that shows that the threshold separating tonic and burst discharge can be represented as a saddle-node bifurcation. The interaction between dendritic K(+) current and I(NaP) provides a physiological explanation for a variable time scale of bursting dynamics characteristic of such a bifurcation.

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PubMedDate not supplied

Type I burst excitability.

We introduce the concept of "type I burst excitability", which is a generalization of the "normal" excitability that is well-known in cardiac and neural systems. We demonstrate this type of burst excitability in a specific model system, a pyramidal cell from the electrosensory lateral line lobe of the weakly electric fish Apteronotus leptorhynchus. As depolarizing current is increased, a saddle-node bifurcation of periodic orbits occurs, which separates tonic and burst activity. This bifurcation is responsible for the excitable nature of the system, and is the basis for the "type I" designation. We verify the existence of this transition from in vitro recordings of a number of actual pyramidal cells. A scaling relationship between the magnitude and duration of a current pulse required to induce a burst is derived. We also observe this type of burst excitability and the scaling relationships in a multicompartmental model that is driven by realistic stochastic synaptic inputs mimicking sensory input. We conclude by discussing the relevance of burst excitability to communication between weakly electric fish.

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