| We introduce a physiology-based neuronal model of sleep-wake cycles, which considers a novel mechanism for a homeostatic regulation of sleep. We propose that the homeostatic sleep process depends on the synaptic transmission of a neuropeptide hypocretin/orexin, which is weakening during wake state due to spiking of hypocretin/orexin-producing neurons and is recovering during silent sleep state. To examine these mechanisms we use a minimal approach which includes a reciprocal connection between a hypocretin/orexin neuron and a local glutamate neuron. The simulation results have shown that such a feedback loop with the spike-dependent reduction of hypocretin/orexin synaptic transmission activated by the circadian process can reproduce not only the sleep-wake neuronal activity but also the principle responses to the external stimulation, such as awakening stimuli in the different phases of homeostatic recovery. These results confirm that a weakening of hypocretin/orexin synaptic transmission may be a mechanism for a homeostatic regulation of sleep, although more processes can be involved. This modeling approach provides a tool for further extensions and examination of interactions between various sleep-related brain nuclei and neurotransmitters systems on neuronal, synaptic and functional levels. |
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