Why can’t you sleep well as you get older From Explanation of Science

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As you get older, it becomes more and more difficult to get a good sleep. According to the survey, the elderly wake up 3-4 times every night on average, and 44% of them have insomnia at night. Many people are troubled by difficulties in falling asleep, shallow sleep and sleep fragmentation, among which sleep fragmentation is the most common sleep problem among the elderly. Why is sleep instability associated with aging? Understanding the potential biological mechanism of this situation may provide new enlightenment for improving the sleep quality of the elderly.

Recently, the Luis de lecea team at Stanford University uncovered the neural mechanism leading to sleep fragmentation and determined how the brain neural mechanism regulating sleep and wakefulness degenerates over time in aging mice. Relevant research results were published in the well-known journal Science on February 25 with a research paper entitled “hyperexcitable aromatic circuits drive sleep installation during aging”.

图滴: https://www.science.org/doi/10.1126/science.abh3021

Orexin (ox), also known as hypothalamic secretin (Hcrt), is a general term for two different neuropeptide hormones. Orexin has a highly excitatory effect, and its main function is to control sleep and wakefulness. To keep us awake, orexin stimulates other neurons to release alerting neurotransmitters such as dopamine, serotonin and norepinephrine.

Therefore, blocking the effect of orexin has become a method to treat sleep disorders. For example, double orexin receptor antagonist (Dora) is a new prescription sleep aid for human orexin system. These drugs act as orexin receptor antagonists to block the role of orexin in the body, so as to promote sleep.

Based on the role of orexin in controlling sleep and wakefulness, Luis de lecea’s team hypothesized in this study that the decline in sleep quality may be due to problems in the neural circuits that control sleep and wakefulness. The researchers explored whether the intrinsic excitability of orexin neurons changed during aging, resulting in the brain’s inability to stably control sleep and waking state, resulting in sleep fragmentation.

Hyperactivity of orexin neurons during aging leads to sleep instability

The team selected young (3 to 5 months) and old mice (18 to 22 months) as experimental subjects, used light carried by fibers to stimulate specific neurons, and recorded the experimental results using imaging technology.

The researchers compared sleep and wakefulness patterns between young and old wild-type mice implanted with electroencephalogram (EEG) – electromyography (EMG) electrodes. In older mice, awake and non REM sleep were more dispersed. After determining the number of orexin neurons in these mice, the team found that older mice lost about 38% of orexin neurons compared with younger mice. This suggests that orexin neurons are more vulnerable in the aging brain.

The research team further used fiber photometry to monitor the internal activity of orexin neurons in young and old mice, and found that the change range of calcium imaging gcamp6f in the old group was smaller, indicating that orexin neurons in old mice were more likely to be excited and triggered, resulting in these old mice waking up more easily. In the same recording time of the same circadian rhythm stage, the average duration of sleep and awakening of elderly mice is shorter, which indicates that the fragmented sleep pattern is age-related. In addition, the correlation analysis of linear fitting showed that the shortening of sleep time may be caused by the hyperactivity of orexin neurons.

Spontaneous appetite activity in young / awake mice

To directly determine whether the intrinsic excitability of orexin neurons changes with age, the researchers recorded the spontaneous activity of orexin neurons in brain slices of young and old mice. The results showed that compared with the orexin neurons of young mice, the elderly orexin neurons showed a higher proportion of spontaneous discharge. At the same time, a series of relevant research data further show that the over excitability of orexin neurons appears with age.

Whole cell patch clamp recording revealed overexcitation of orexin neurons in the elderly

KCNQ potassium channel is a biological switch crucial to the function of many cells. KCNQ2 and KCNQ3 subtypes pair to form KCNQ2 / 3 heterotetramer, which mainly constitutes the molecular substrate (IM) of M current, and plays a key role in controlling subthreshold excitability, repolarization and synaptic sensitivity of neurons.

Based on this, the research team applied KCNQ2 / 3 channel selective regulator to brain slices of young or old mice. The results showed that the basal im of orexin neurons in old mice was significantly smaller than that in young mice, which was verified by array tomography at ultrastructural resolution, which showed that the immunoreactivity of KCNQ2 in orexin neurons in old mice decreased significantly, and the degradation of KCNQ2 pathway resulted in the damage of M current in orexin neurons during aging.

Sleep fragmentation is associated with the loss of KCNQ2 in orexin neurons in the elderly

This study shows that during aging, the degradation of potassium channels leads to over excitation of orexin neurons, resulting in sleep instability. Continuous targeted treatment of potassium channels in elderly mice can improve the sleep quality of mice. This provides potential therapeutic ideas for solving human sleep problems and helps to develop more targeted therapies.

参考: https://www.science.org/doi/10.1126/science.abh3021

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