Abstract
Intrinsic Neuronal Excitability: A Role in Homeostasis and Disease
Highlights
Beraneck and Idoux (2012) detail evidence to support the hypothesis that changes in background discharge during vestibular compensation of vestibular nucleus neurons appears to be predominately expressed as changes in the excitability of the type B medial vestibular nucleus (MVN) neuron subpopulation
Changes in the number of voltage-gated sodium (Na+) channels have been demonstrated in animal models of chronic pain
These changes in dorsal root ganglion (DRG) neuron intrinsic excitability, presumably underlie the hyperalgesia and allodynia commonly observed in chronic pain models
Summary
Beraneck and Idoux (2012) detail evidence to support the hypothesis that changes in background discharge during vestibular compensation of vestibular nucleus neurons appears to be predominately expressed as changes in the excitability of the type B medial vestibular nucleus (MVN) neuron subpopulation. Changes in the number of voltage-gated sodium (Na+) channels have been demonstrated in animal models of chronic pain.
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