Non-threatening familiar sounds can go unnoticed during sleep despite the fact that they
enter our brain by exciting the auditory nerves. Extracellular cortical recordings in the primary
auditory cortex of rodents show that an increase in firing rate in response to pure tones during
deep phases of sleep is comparable to those evoked during wakefulness. This result challenges the
hypothesis that during sleep cortical responses are weakened through thalamic gating. An alternative
explanation comes ...
Non-threatening familiar sounds can go unnoticed during sleep despite the fact that they
enter our brain by exciting the auditory nerves. Extracellular cortical recordings in the primary
auditory cortex of rodents show that an increase in firing rate in response to pure tones during
deep phases of sleep is comparable to those evoked during wakefulness. This result challenges the
hypothesis that during sleep cortical responses are weakened through thalamic gating. An alternative
explanation comes from the observation that the spatiotemporal spread of the evoked activity by
transcranial magnetic stimulation in humans is reduced during non-rapid eye movement (NREM)
sleep as compared to the wider propagation to other cortical regions during wakefulness. Thus,
cortical responses during NREM sleep remain local and the stimulus only reaches nearby neuronal
populations. We aim at understanding how this behavior emerges in the brain as it spontaneously
shifts between NREM sleep and wakefulness. To do so, we have used a computational neural-mass
model to reproduce the dynamics of the sensory auditory cortex and corresponding local field
potentials in these two brain states. Following the synaptic homeostasis hypothesis, an increase in
a single parameter, namely the excitatory conductance g¯AMPA, allows us to place the model from
NREM sleep into wakefulness. In agreement with the experimental results, the endogenous dynamics
during NREM sleep produces a comparable, even higher, response to excitatory inputs to the ones
during wakefulness. We have extended the model to two bidirectionally connected cortical columns
and have quantified the propagation of an excitatory input as a function of their coupling. We have
found that the general increase in all conductances of the cortical excitatory synapses that drive the
system from NREM sleep to wakefulness does not boost the effective connectivity between cortical
columns. Instead, it is the inter-/intra-conductance ratio of cortical excitatory synapses that should
raise to facilitate information propagation across the brain.
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