A team of researchers led by Dr. WANG Liping from the Shenzhen Institute of Advanced Technology (SIAT) of the Chinese Academy of Sciences recently reported a common circuit that regulates both innate fear and rapid eye movement (REM) sleep.
As specified in a Eurek Alert! report, REM sleep brings about brief yet periodic awakenings. Specifically, in 1966, Dr. Frederic Snyder reported the "sentinel" role of REM could help animals be ready for a fight or flight reaction against potential predator attacks. However, up till now, there has been no investigational evidence for this assumption.
In that particular experiment, the animals slept in a sealed chamber. They were also exposed to TMT (trimethylthiazoline) odor, a stimulus specifying a predator's presence.
Dr. Wang explained TMT stimulated rapid arousal from REM sleep although not from non-rapid-eye movement sleep. It then proposes that REM sleep has particular properties that enable rapid arousal "in response to predatory stimuli."
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Rapid Eye Movement Sleep
As REM is mostly characterized by higher arousal thresholds compared to non-rapid-eye-movement (NREM) sleep, the research group aimed to unveil the neural mechanisms that underlie this REM-particular function.
In their study published in the Neuron journal, the researchers investigated the "medial subthalamic nucleus (mSTN), a brain region containing a high density of CRH or corticotropin-releasing hormone neurons.
Through the combination of vivo neural activity recording and cell-type particular manipulations, they discovered that mSTN-CRH neurons generated a lowered arousal threshold during REM sleep to detect predator threats and amplified defensive reactions following awakening.
Such results showed that sustained predator exposure induced a substantial rise in total REM sleep although briefer durations of distinctive REM-sleep episodes and "sleep architecture fragmentation."
The American Sleep Association describes this specific stage of sleep as "paradoxical sleep," or "desynchronized sleep" because of the physiological differences to the waking states of a person, including rapid, desynchronized, and low-voltage brainwaves.
It has been believed that both the electrical and chemical activities regulating this sleep phase originate in the brain stem, and is most notably characterized by a mixture of neurotransmitter and monoamine neurotransmitters.
mSTN-CRH Neurons
Essentially, mSTN-CRH neurons are needed for this adaptation of the REM sleep to exposure to chronic threat. It is an instance of how evolution results in two unique yet related roles for the same set of neurons instead of a pair of complete separate neural networks.
Commenting on their findings, Dr. Wang said they might hypothesize that natural selection favors optimizing current neural circuity for efficacy in indication transduction and energy use over metabolically costlier solutions.
The co-occurrence of augmented REM sleep and stress-associated mood disorders has been observed in clinical experiments.
The new findings of this research provide a possible evolutionary explanation of such a phenomenon and explain the fundamental neurobiological mechanism.
According to the lead author of the study, Dr. Yu-Ting Tseng, their study raises the question of whether there is a possibility of treating mood disorders "by targeting the common regulatory" sleep circuit of fear and sleep. He added that they would continue their work to find answers to the question.
Related information about rapid eye movement sleep is shown on MyWorkplaceHealth's YouTube video below:
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