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Chaotic dynamics underpins the slow oscillation of general anesthesia and nonREM sleep
© Steyn-Ross et al; licensee BioMed Central Ltd. 2012
- Published: 16 July 2012
- Phase Coherence
- Slow Oscillation
- nonREM Sleep
- Inhibitory Postsynaptic Potential
- Cortical Model
Electrical recordings of brain activity show that entry into anesthetic unconsciousness is signposted by the emergence of large, slow oscillations of electrical activity (~1 Hz) that appear very similar to the slow waves observed in natural sleep. In this phase, populations of cortical neurons periodically switch between hyperpolarized inactivity (“down” state), and wake-like depolarized activation (“up” state) . The origin of the slow oscillation has not yet been unambiguously established, and remains an area of intense research and debate [2, 3]. Here we suggest a novel mechanism in which the up- and down-states are generated spontaneously by emergent chaotic waves of spatiotemporal activity that sweep the cortex. We present a mean-field model of the cortex in which populations of neurons are densely interlinked by both chemical synapses—including idealized long-range spatially heterogeneous connections—and by direct electrical connections forming a continuous network of interneuronal gap junctions. Anesthetic effect is modeled as a moderate reduction in inhibitory diffusion, paired with an increase in inhibitory postsynaptic potential. We explore model dynamics in the vicinity of a general-anesthetic induced transition from wake to coma. In this region the system is poised at a codimension-2 point where competing Turing (spatial) and Hopf (temporal) instabilities co-exist. We argue that normal functioning of the resting “default-wake” brain requires a delicate balance between these instabilities. Reduction of gap-junction diffusivity disturbs the balance in favor of the Hopf instability, eventually predicting global seizure in the limit of severe imbalance.
A spontaneous, spatiotemporally chaotic state—generated by nonlinear Turing–Hopf interaction—is the underlying mechanism for the slow oscillation observed in general anesthesia. A similar transition to low-frequency chaos may also occur in natural nonREM sleep, and if so, may have significant implications for synaptic downscaling and memory processing hypothesized to occur during deep sleep.
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This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.