FRIDAY, Oct. 26 (HealthDay News) -- Inhaled anesthetics work not only by shutting down networks that are active during natural wakefulness, but also by activating brain networks that are active during natural sleep, according to an experimental study published online Oct. 25 in Current Biology.
To examine whether volatile anesthetics such as isoflurane and halothane function by recruiting the brain's natural sleep circuitry, Jason T. Moore, from Children's Hospital of Philadelphia, and colleagues investigated the role of the ventrolateral preoptic nucleus (VLPO) in the hypothalamus, which contains neurons that preferentially fire during natural sleep.
Through electrophysiological and other studies in mice, the researchers found that isoflurane and halothane increased the number of active neurons in the VLPO, and the neurons activated by these anesthetics were the subpopulation responsible for promoting natural sleep. VLPO neurons were only activated when the mice were sedated or unconscious, and destroying these neurons led to acute resistance to isoflurane-induced hypnosis. Isoflurane did not affect non-sleep active VLPO neurons. The anesthesia-induced depolarization of VLPO neurons was not only due to presynaptic inhibition of wake-active neurons, but also involved a direct postsynaptic effect on the neurons, which resulted from the closing of background potassium conductance.
"Cumulatively, this work demonstrates that anesthetics are capable of directly activating endogenous sleep-promoting networks and that such actions contribute to their hypnotic properties," Moore and colleagues conclude.
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