Acetylcholine and synaptic homeostasis
© Fink et al; licensee BioMed Central Ltd. 2012
Published: 16 July 2012
The synaptic renormalization hypothesis posits that a primary function of sleep is to maintain synaptic homeostasis . According to this theory, the flood of sensory signals processed by the brain during waking results in global potentiation of cortical synapses, a process which consumes energy and space and therefore cannot continue unabated. Sleep is therefore a period of global synaptic downscaling that maintains homeostasis, thereby conserving energy and cortical space. Specifically, it is slow-wave activity (SWA) during NREM sleep that is thought to induce this depotentiation. While evidence in support of both global potentiation of synapses during waking  and SWA-mediated downscaling of synapses during sleep  continues to mount, there is still much uncertainty about the biophysical mechanisms which may contribute to either synaptic upscaling or downscaling .
Counter-intuitively, the global potentiation induced by the presence of ACh in our simulated networks is due to asynchronous activity. This is due to the fact that in the asynchronous state, there exists important statistical structure to the network dynamics, so that post-synaptic neurons are more likely to fire immediately after (rather than before) a pre-synaptic action potential, thus leading to net potentiation of the network due to STDP.
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