Cell Types, Network Homeostasis, and Pathological Compensation from a Biologically Plausible Ion Channel Expression Model
By Timothy O’Leary, Alex H. Williams, Alessio Franci, Eve Marder. 2014
125 citations recorded by the source corpus.
SUMMARY How do neurons develop, control, and maintain their electrical signaling properties in spite of ongoing protein turnover and perturbations to activity? From generic assumptions about the molecular biology underlying channel expression, we derive a simple model and show how it encodes an “activity set point” in single neurons. The model generates diverse self-regulating cell types and relates correlations in conductance expression observed in vivo to underlying channel expression rates. Synaptic as well as intrinsic conductances can be regulated to make a self-assembling central pattern generator network; thus, network-level homeostasis can emerge from cell-autonomous regulation rules. Finally, we demonstrate that the outcome of homeostatic regulation depends on the complement of ion channels expressed in cells: in some cases, loss of specific ion channels can be compensated; in others, the homeostatic mechanism itself causes pathological loss of function.
Subfields: Cellular and Molecular Neuroscience, Cognitive Neuroscience, Molecular Biology
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Citations in the corpus
- Homeostatic Activity-Dependent Tuning of Recurrent Networks for Robust Propagation of Activity (2015, background): “Theoretical modulation rules have been successfully applied to the regulation of motor output in the stomatogastric nervous system of crustaceans (LeMasson et al., 1993; Liu et al., 1998; Marder and Goaillard, 2006; O’Leary et al., 2014).”