AI Article Synopsis
- The study investigates how certain brainstem circuits control eye movements and adapt behavior through intrinsic and synaptic plasticity.
- It highlights that firing rate potentiation, driven by changes in specific potassium currents, plays a key role in compensating for inner ear dysfunction during optokinetic reflexes.
- The research demonstrates that in normal mice, the system adapts well to vestibular loss, while mice lacking BK channels show significant impairments in restoring normal eye movement, suggesting intrinsic excitability is crucial for adaptive behavior.
Article Abstract
Neural circuits are endowed with several forms of intrinsic and synaptic plasticity that could contribute to adaptive changes in behavior, but circuit complexities have hindered linking specific cellular mechanisms with their behavioral consequences. Eye movements generated by simple brainstem circuits provide a means for relating cellular plasticity to behavioral gain control. Here we show that firing rate potentiation, a form of intrinsic plasticity mediated by reductions in BK-type calcium-activated potassium currents in spontaneously firing neurons, is engaged during optokinetic reflex compensation for inner ear dysfunction. Vestibular loss triggers transient increases in postsynaptic excitability, occlusion of firing rate potentiation, and reductions in BK currents in vestibular nucleus neurons. Concurrently, adaptive increases in visually evoked eye movements rapidly restore oculomotor function in wild-type mice but are profoundly impaired in BK channel-null mice. Activity-dependent regulation of intrinsic excitability may be a general mechanism for adaptive control of behavioral output in multisensory circuits.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5575767 | PMC |
| http://dx.doi.org/10.1016/j.neuron.2016.11.019 | DOI Listing |
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