Study reveals neural mechanism of stress-induced anxiety and metabolic abnormalities

On March 22, Yang Fan's research group from the Institute of Brain Cognition and Brain Diseases, Shenzhen Institutes of Advanced Technology, Chinese Academy of Sciences, and Shenzhen-Hong Kong Brain Science Innovation Institute published a paper entitled Cav3.
1-driven bursting firing in ventromedial hypothalamic neurons in Molecular Psychiatry.
The research results exerts dual control of anxiety-like behavior and energy expenditure, revealing that the cluster discharge of ventromedial hypothalamus (VMH) neurons in chronic stress stress regulates anxiety and energy metabolism, while The calcium channel Cav3.
1 plays an important role in the above regulation
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The research results not only deeply analyze the neural mechanism of stress-induced anxiety and metabolic abnormalities, but also provide new intervention strategies for intervening anxiety and stress-related diseases
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Anxiety caused by stress is a common emotional state, but long-term chronic anxiety not only affects mental health, but also has serious negative effects on the body's physiological functions
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A lot of evidence shows that when you are in a state of excessive anxiety and stress for a long time, the sympathetic nerves of the body will be overexcited and lead to physiological homeostasis such as abnormal glucose and lipid metabolism, endocrine disorders, bone loss, etc.
However, stress stress affects anxiety and metabolism.
The neural mechanism is still not fully understood
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In addition, a series of studies in recent years have also found that VMH can play an important role in the regulation of anxiety and metabolism, but the neural mechanism of its neurons regulating anxiety and energy metabolism under stress also needs to be further analyzed
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Through research, the research team found that chronic stress-stressed mice exhibited anxiety-like behaviors and abnormal metabolic balance (reduced food intake, decreased energy expenditure), and the proportion and intensity of cluster-firing neurons in the VMH were also significantly increased
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Using optogenetic techniques to modulate VMH neurons can induce cluster firing and enhanced VMH calcium activity, and sustained-evoked cluster firing can mimic chronic stress-like anxiety-like behaviors and metabolic changes
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In order to further verify the mechanism of cluster discharge, the research team used in vitro electrophysiology, in vivo drug administration, RNAi interference and other technologies to find that calcium channel Cav3.
1 can mediate cluster discharge in VMH neurons, and the expression of Cav3.
1 decreased It can significantly reduce the proportion of cluster-firing neurons in the VMH of anxious mice, thereby alleviating anxiety-like behavior and metabolic abnormalities in mice
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In addition, the anti-anxiety drug, fluoxetine, taken for a long time in chronic stress-stressed mice can reduce the proportion of cluster-firing neurons, block chronic stress-induced anxiety, and alleviate abnormal peripheral energy metabolism
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The research team has been conducting research on the mechanism of the central nervous system regulating bone metabolism for a long time.
Earlier, co-authors found that VMH is involved in the neural circuit of chronic stress-induced anxiety and bone loss (Journal of Clinical Investigation, 2020), and light regulates the secretion of parathyroid hormone.
Intervention in bone loss (Nature Communications, 2022)
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Relevant research work has been supported by the National Natural Science Foundation of China, the Chinese Academy of Sciences, Guangdong Province and Shenzhen
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0VMH neuron cluster firing regulates anxiety-like behavior and energy metabolism Source: Shenzhen Institutes of Advanced Technology, Chinese Academy of Sciences