Previously, Academician Yan Ning posted on Weibo to congratulate the first senior PI he invited for returning to China to join the Shenzhen Academy of Medical Sciences. On May 26, 2025, the Shenzhen Academy of Medical Sciences officially announced that Professor Danyang, an academician of the National Academy of Sciences and an academician of the American Academy of Arts and Sciences, will join the institute full-time in June 2025.

As an internationally renowned neuroscientist, Professor Danyang has been
deeply engaged in the fields of visual neuroscience and sleep neural mechanisms
for many years. His research results have been published in top academic
journals such as Cell, Nature Neuroscience, and Science Advanceds, opening up a
new perspective for understanding brain functions. Recently, she has published a
major research in Cell, so let us focus on its latest scientific research
results together.
Cell
On June 24, 2025, Professor Danyang's team published a research paper
entitled "Neuroendocrine circuit for sleep-dependent growth hormone release" in
the top international journal Cell.

Sleep is crucial to the recovery of the body and brain. Deficiency of sleep
can cause health problems such as diabetes and obesity, and its impact on
tissues and organs is partially achieved through neuroendocrine regulation.
Growth hormone (GH) can promote growth and regulate metabolism, while GH
deficiency is similar to the adverse consequences of sleep deprivation, and GH
release is closely related to sleep, but the neural mechanisms of the
interaction between the two have not been elucidated.
Through optogenetic and chemical genetic techniques, combined with calcium
imaging and electrode recording, the research team found that the activity of
hypothalamic GHRH and SST neurons in the sleep-awakened state regulates GH
release: arcuate nuclear SST neurons inhibit GHRH neurons, and periventricular
SST neurons projected to the median bulge, jointly inhibiting GH release, while
the activity patterns of GHRH and SST in REM and NREM are different in sleep. In
addition, it was found that GH promotes awakening by enhancing the excitability
of the locus neurons, revealing the bidirectional neural circuit mechanism of
sleep and hormone regulation.

Science Advances
On January 17, 2025, Professor Danyang's research team published a research
paper entitled "Activation of locus coeruleus noradrenergic neurons rapidly
drives homeostatic sleep pressure" in the journal Science Advanceds.
The study revealed through a series of experiments that the activation of
norepinephrine neurons in the locustrine nucleus rapidly triggers sleep
homeostasis stress.

Homeostasis regulation of sleep is crucial to maintaining brain recovery
function. Its mechanism involves adenosine accumulation, synaptic enhancement,
etc., but the specific role of each mechanism in the natural sleep cycle is
still unclear. The locustrine nucleus (LC) norepinephrine neurons are key
arousal-pro-awakening nerve groups, but whether their activities are involved in
the formation of sleep stress through "functional fatigue" has not been
systematically studied.
The research team used optogenetics and fiber optic photometry to find that
activating LC neurons can quickly increase sleep tendencies after brief
awakening, which is different from other pro-awakening neurons. Repeated
stimulation results in a sharp decline in calcium activity and intracerebral
norepinephrine (NE) release in LC neurons, while knockdown of α2A adrenergic
receptors inhibits this decline and prolongs awakening, confirming that α2A
receptor-mediated NE autoinhibition is involved in this process. This study
reveals that the “functional fatigue” of LC neurons becomes a new mechanism for
the formation of sleep stress by reducing the ability to promote awakening.
Nature neuroscience
On January 18, 2024, Professor Danyang's research team published "Microglia regulate sleep through calcium-dependent modulation of norepinephrine transmission" in the journal Nature neuroscience. This study revealed through a series of experiments that microglia regulate sleep through norepinephrine transmission regulation that relies on calcium signal.

Sleep is crucial for the maintenance of brain homeostasis (such as
regulation of neuronal activity and removal of metabolic waste), and microglia,
as the main immune cells in the brain, play a key role in synaptic pruning and
neuroprotection. Both sleep disorders and microglia abnormalities are associated
with neurodegenerative diseases, but the interaction mechanism between the two
is still unclear. Metabolic substances (such as ATP, adenosine) and cytokines
are known to regulate sleep, while microglia-expressed P2Y12 receptor
(Gi-coupled GPCR) responds to these molecules, suggesting that they may be
involved in sleep regulation.
The research team used microglia-specifically labeled Tmem119-CreERT2 mice,
combined with chemical genetics, two-photon imaging and biosensor technology, to
find that microglia regulate sleep through the P2Y12–Gi signaling pathway:
activation of this signal can increase the intracellular Ca²⁺ levels, inhibit
norepinephrine transmission and increase adenosine concentration, thereby
promoting sleep; during natural sleep switching, a decrease in norepinephrine
levels will also induce an increase in microglia Ca²⁺. Conversely, blocking
P2Y12–Gi signal or Ca²⁺ elevation reduces sleep. This study reveals a new
mechanism by which microglia regulate sleep through the interaction of Ca²⁺
signal with the norepinephrine-adenosine system.
The joining of Academician Danyang has injected strong impetus into the
Shenzhen Academy of Medical Sciences in the field of sleep and consciousness
research. As the research team led by her in-depth exploration, these
cutting-edge research results will not only promote human understanding of the
mysteries of the brain, but also hope to bring new dawn to the prevention and
treatment of major health problems such as sleep disorders and neurodegenerative
diseases, and help my country move to a higher international level in the field
of brain science research.