Bio
Yanan completed her Ph.D. degree at Fudan University, where she uncovered the mechanisms of sleep transitions from the evolutionary point of view in Dr Zhili Huang’s lab, with a combination of optogenetics, in vivo electrophysiology, fiber photometry, polysomnography, immunohistochemistry and so on. In the de Lecea lab, Yanan is now curious about how sleep regulates the balance between DNA damage and repair with approaches of imaging. At the same time, she is interested in larger scale imaging during different brain states. Outside the lab, Yanan enjoys biking and exploring the sunny bay area.
Honors & Awards
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First Prize of Academic Scholarship, Fudan University (2019)
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First Prize of Academic Scholarship, Fudan University (2017)
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Outstanding Graduates Awards., Taiyuan University of Technology (2016)
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Chancellor's Scholarship Nomination Award., Taiyuan University of Technology (2015)
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First Prize of the 13th Extracurricular Academic Science and Technology Works Competition., Taiyuan University of Technology (2015)
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Professional Study Scholarships., Taiyuan University of Technology (2014 and 2016)
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Third Prize of National Collegiate Mathematical Modeling Competition, Shanxi Division, Taiyuan University of Technology (2014)
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First Prize of National Collegiate Mathematics Competition Preliminary Round, Taiyuan University of Technology (2013)
Professional Education
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Bachelor, Taiyuan University of Technology, Bioengineering (2016)
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Ph.D., Fudan University, Pharmacology (2022)
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Postdoc, Stanford University, Biomedical Sciences
All Publications
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GABAergic neurons in the rostromedial tegmental nucleus are essential for rapid eye movement sleep suppression.
Nature communications
2022; 13 (1): 7552
Abstract
Rapid eye movement (REM) sleep disturbances are prevalent in various psychiatric disorders. However, the neural circuits that regulate REM sleep remain poorly understood. Here, we found that in male mice, optogenetic activation of rostromedial tegmental nucleus (RMTg) GABAergic neurons immediately converted REM sleep to arousal and then initiated non-REM (NREM) sleep. Conversely, laser-mediated inactivation completely converted NREM to REM sleep and prolonged REM sleep duration. The activity of RMTg GABAergic neurons increased to a high discharge level at the termination of REM sleep. RMTg GABAergic neurons directly converted REM sleep to wakefulness and NREM sleep via inhibitory projections to the laterodorsal tegmentum (LDT) and lateral hypothalamus (LH), respectively. Furthermore, LDT glutamatergic neurons were responsible for the REM sleep-wake transitions following photostimulation of the RMTgGABA-LDT circuit. Thus, RMTg GABAergic neurons are essential for suppressing the induction and maintenance of REM sleep.
View details for DOI 10.1038/s41467-022-35299-x
View details for PubMedID 36477665
View details for PubMedCentralID PMC9729601
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A cluster of mesopontine GABAergic neurons suppresses REM sleep and curbs cataplexy.
Cell discovery
2022; 8 (1): 115
Abstract
Physiological rapid eye movement (REM) sleep termination is vital for initiating non-REM (NREM) sleep or arousal, whereas the suppression of excessive REM sleep is promising in treating narcolepsy. However, the neuronal mechanisms controlling REM sleep termination and keeping sleep continuation remain largely unknown. Here, we reveal a key brainstem region of GABAergic neurons in the control of both physiological REM sleep and cataplexy. Using fiber photometry and optic tetrode recording, we characterized the dorsal part of the deep mesencephalic nucleus (dDpMe) GABAergic neurons as REM relatively inactive and two different firing patterns under spontaneous sleep-wake cycles. Next, we investigated the roles of dDpMe GABAergic neuronal circuits in brain state regulation using optogenetics, RNA interference technology, and celltype-specific lesion. Physiologically, dDpMe GABAergic neurons causally suppressed REM sleep and promoted NREM sleep through the sublaterodorsal nucleus and lateral hypothalamus. In-depth studies of neural circuits revealed that sublaterodorsal nucleus glutamatergic neurons were essential for REM sleep termination by dDpMe GABAergic neurons. In addition, dDpMe GABAergic neurons efficiently suppressed cataplexy in a rodent model. Our results demonstrated that dDpMe GABAergic neurons controlled REM sleep termination along with REM/NREM transitions and represented a novel potential target to treat narcolepsy.
View details for DOI 10.1038/s41421-022-00456-5
View details for PubMedID 36280664
View details for PubMedCentralID PMC9592589
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Whole-Brain Monosynaptic Afferents to Rostromedial Tegmental Nucleus Gamma-Aminobutyric Acid-Releasing Neurons in Mice.
Frontiers in neuroscience
2022; 16: 914300
Abstract
Increasing evidence has revealed that the rostromedial tegmental area (RMTg) mediates many behaviors, including sleep and addiction. However, presynaptic patterns governing the activity of γ-aminobutyric acid-releasing (GABAergic) neurons, the main neuronal type in the RMTg, have not been defined. Here, we used cell-type-specific retrograde trans-synaptic rabies viruses to map and quantify the monosynaptic afferents to RMTg GABAergic neurons in mouse whole brains. We identified 71 ascending projection brain regions. Sixty-eight percent of the input neurons arise from the ipsilateral and 32% from the contralateral areas of the brain. The first three strongest projection regions were the ipsilateral lateral hypothalamus, zone incerta, and contralateral pontine reticular nucleus. Immunohistochemistry imaging showed that the input neurons in the dorsal raphe, laterodorsal tegmentum, and dorsal part of zone incerta were colocalized with serotoninergic, cholinergic, and neuronal nitric oxide synthetase-expressing neurons, respectively. However, in the lateral hypothalamus, a few input neurons innervating RMTg GABAergic neurons colocalized orexinergic neurons but lacked colocalization of melanin-concentrating hormone neurons. Our findings provide anatomical evidence to understand how RMTg GABAergic neurons integrate diverse information to exert varied functions.
View details for DOI 10.3389/fnins.2022.914300
View details for PubMedID 35733933
View details for PubMedCentralID PMC9207306
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The Rostromedial Tegmental Nucleus: Anatomical Studies and Roles in Sleep and Substance Addictions in Rats and Mice.
Nature and science of sleep
2020; 12: 1215-1223
Abstract
The rostromedial tegmental nucleus (RMTg), a brake of the dopamine system, is specifically activated by aversive stimuli, such as foot shock. It is principally composed of gamma-aminobutyric acid neurons. However, there is no exact location of the RMTg on the brain stereotaxic atlas. The RMTg can be defined by c-Fos staining elicited by psychostimulants, the position of retrograde-labeled neurons stained by injections into the ventral tegmental area (VTA), the terminal field formed by axons from the lateral habenula, and some molecular markers identified as specifically expressed in the RMTg such as FoxP1. The RMTg receives a broad range of inputs and produces diverse outputs, which indicates that the RMTg has multiple functions. First, the RMTg plays an essential role for non-rapid eye movement sleep. Additionally, the RMTg serves a vital role in response to addiction. Opiates increase the firing rates of dopaminergic neurons in the VTA by acting on μ-opioid receptors on RMTg neurons and their terminals inside the VTA. In this review, we summarize the recent research advances on the anatomical location of the RMTg in rats and mice, its projections, and its regulation of sleep-wake behavior and addiction.
View details for DOI 10.2147/NSS.S278026
View details for PubMedID 33380853
View details for PubMedCentralID PMC7769149
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The rostromedial tegmental nucleus is essential for non-rapid eye movement sleep.
PLoS biology
2018; 16 (4): e2002909
Abstract
The rostromedial tegmental nucleus (RMTg), also called the GABAergic tail of the ventral tegmental area, projects to the midbrain dopaminergic system, dorsal raphe nucleus, locus coeruleus, and other regions. Whether the RMTg is involved in sleep-wake regulation is unknown. In the present study, pharmacogenetic activation of rat RMTg neurons promoted non-rapid eye movement (NREM) sleep with increased slow-wave activity (SWA). Conversely, rats after neurotoxic lesions of 8 or 16 days showed decreased NREM sleep with reduced SWA at lights on. The reduced SWA persisted at least 25 days after lesions. Similarly, pharmacological and pharmacogenetic inactivation of rat RMTg neurons decreased NREM sleep. Electrophysiological experiments combined with optogenetics showed a direct inhibitory connection between the terminals of RMTg neurons and midbrain dopaminergic neurons. The bidirectional effects of the RMTg on the sleep-wake cycle were mimicked by the modulation of ventral tegmental area (VTA)/substantia nigra compacta (SNc) dopaminergic neuronal activity using a pharmacogenetic approach. Furthermore, during the 2-hour recovery period following 6-hour sleep deprivation, the amount of NREM sleep in both the lesion and control rats was significantly increased compared with baseline levels; however, only the control rats showed a significant increase in SWA compared with baseline levels. Collectively, our findings reveal an essential role of the RMTg in the promotion of NREM sleep and homeostatic regulation.
View details for DOI 10.1371/journal.pbio.2002909
View details for PubMedID 29652889
View details for PubMedCentralID PMC5919677