Activity-independent homeostasis in rhythmically active neurons - PubMed (original) (raw)
Comment
. 2003 Jan 9;37(1):109-20.
doi: 10.1016/s0896-6273(02)01104-2.
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- PMID: 12526777
- DOI: 10.1016/s0896-6273(02)01104-2
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Comment
Activity-independent homeostasis in rhythmically active neurons
Jason N MacLean et al. Neuron. 2003.
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Abstract
The shal gene encodes the transient potassium current (I(A)) in neurons of the lobster stomatogastric ganglion. Overexpression of Shal by RNA injection into neurons produces a large increase in I(A), but surprisingly little change in the neuron's firing properties. Accompanying the increase in I(A) is a dramatic and linearly correlated increase in the hyperpolarization-activated inward current (I(h)). The enhanced I(h) electrophysiologically compensates for the enhanced I(A), since pharmacological blockade of I(h) uncovers the physiological effects of the increased I(A). Expression of a nonfunctional mutant Shal also induces a large increase in I(h), demonstrating a novel activity-independent coupling between the Shal protein and I(h) enhancement. Since I(A) and I(h) influence neuronal activity in opposite directions, our results suggest a selective coregulation of these channels as a mechanism for constraining cell activity within appropriate physiological parameters.
Comment on
- Current compensation in neuronal homeostasis.
Marder E, Prinz AA. Marder E, et al. Neuron. 2003 Jan 9;37(1):2-4. doi: 10.1016/s0896-6273(02)01173-x. Neuron. 2003. PMID: 12526765 Review.
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