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On May 7, 2021, Molecular Psychiatry, the top journal in the field of neuropsychiatric diseases, held a special session in China: 7 consecutive publications of the research results of Chinese scientists online, demonstrating the strength of China's scientific research! Liver X receptor (LXR) is a member of the metabolic nuclear receptor family, two subtypes of LXRα and LXRβ.
LXRα is mainly expressed in the liver and intestines, while LXRβ is mainly expressed in the brain.
Studies have shown that after knocking out LXRβ, there are obstacles to nerve regeneration and synapse formation in the hippocampus.
The activation of LXRβ signal can rebalance the excitatory and inhibitory synaptic transmission in the amygdala brain area, thereby reducing anxiety-like behaviors.
Studies have shown that LXRβ can affect the differentiation of radial glial cells (RGC) into astrocytes or oligodendrocytes.
In the brains of adult rodents, astrocytes accumulate large amounts of glutamate through glutamate transporter 1 (GLT-1).
Astrocytes are an important part of synaptic transmission, and their dysfunction leads to neuropsychiatric diseases such as anxiety and depression.
On May 7, 2021, Professor Fan Xiaotang from the School of Psychology of the Third Military Medical University published a paper revealing that LXRβ derived from astrocytes regulates anxiety through excitatory and inhibitory synaptic balance mechanisms.
LXRβ-GFAP knockout mice showed anxiety-like behavior disorder.
Researchers specifically knocked out LXRβ on astrocytes (hereinafter referred to as LXRβ-GFAP knockout mice) to cause anxiety-like behavior in adult mice.
The amygdala, mPFC, hypothalamus, hippocampus and other brain areas are the key brain areas that regulate anxiety, but in LXRβ-GFAP knockout mice, only the expression of LXRβ in the mPFC brain area is reduced.
LXRβ-GFAP knockout mice synapse proteins change excitatory/inhibitory synaptic disorders are the key mechanism of anxiety.
They found that the expression of excitatory synapse protein in the brain region of mPFC in LXRβ-GFAP knockout mice was significantly increased, but the inhibitory synapse protein did not change.
More surprisingly, this up-regulation of excitatory synaptic proteins only occurs in the 5th layer of the mPFC brain area.
Electrophysiological experiments have shown that the spontaneous inhibitory postsynaptic currents of neurons in the 5th layer of vertebral bodies have not changed, but spontaneously The excitatory postsynaptic current increases.
This indicates that the region's excitability/inhibitory imbalance is more biased towards excitability.
Virus strategy specifically knocks down LXRβ on astrocytes.
Researchers injected AAV-gfaABC1d-Cre virus into the mPFC region of LXRβ-floxp mice and were able to specifically knock out LXRβ on astrocytes.
Open field experiments, Elevated experiments and light-dark shuttle box experiments show that specific knockout of LXRβ can cause anxiety-like behaviors, and the spontaneous excitatory postsynaptic currents of vertebral neurons are also enhanced.
After being released into the synaptic cleft, the excitatory neurotransmitter glutamate is rapidly absorbed by GLT-1.
However, the expression of GLT-1 protein in mPFC brain regions of LXRβ-GFAP knockout mice and virus knockdown LXRβ mice was reduced.
After intraperitoneal injection of CEF can promote the expression of GLT-1 protein while reducing the spontaneous excitatory postsynaptic current, improving anxiety-like behavior.
Professor Fan Xiaotang’s research group focused on the key scientific issue in developmental biology "the pattern and mechanism of lamellar structure formation", focusing on the development and formation of estrogen receptor β (ERβ) and liver X receptor β (LXRβ) in the brain lamellar structure The role and mechanism of nuclear receptors, as well as the developmental regulatory mechanism of nuclear receptors in neuropsychological abnormalities and neuropsychiatric diseases.
In May 2018, Fan Xiaotang published an article in PNAS and found that after knocking out LXRβ, the formation of progenitor cells in the hippocampal DG area was abnormal and neurogenesis was reduced, causing autism-like behavior disorder.
[References] 1.
https://doi.
org/10.
1038/s41380-021-01139-5 The pictures in the article are all from the references.
If you need to download the original text, you can click on the Baidu web disk link: https://pan.
baidu.
com/ s/1dCtf4pltXiJj7DR1fcgXAw Extraction code: 9mif
On May 7, 2021, Molecular Psychiatry, the top journal in the field of neuropsychiatric diseases, held a special session in China: 7 consecutive publications of the research results of Chinese scientists online, demonstrating the strength of China's scientific research! Liver X receptor (LXR) is a member of the metabolic nuclear receptor family, two subtypes of LXRα and LXRβ.
LXRα is mainly expressed in the liver and intestines, while LXRβ is mainly expressed in the brain.
Studies have shown that after knocking out LXRβ, there are obstacles to nerve regeneration and synapse formation in the hippocampus.
The activation of LXRβ signal can rebalance the excitatory and inhibitory synaptic transmission in the amygdala brain area, thereby reducing anxiety-like behaviors.
Studies have shown that LXRβ can affect the differentiation of radial glial cells (RGC) into astrocytes or oligodendrocytes.
In the brains of adult rodents, astrocytes accumulate large amounts of glutamate through glutamate transporter 1 (GLT-1).
Astrocytes are an important part of synaptic transmission, and their dysfunction leads to neuropsychiatric diseases such as anxiety and depression.
On May 7, 2021, Professor Fan Xiaotang from the School of Psychology of the Third Military Medical University published a paper revealing that LXRβ derived from astrocytes regulates anxiety through excitatory and inhibitory synaptic balance mechanisms.
LXRβ-GFAP knockout mice showed anxiety-like behavior disorder.
Researchers specifically knocked out LXRβ on astrocytes (hereinafter referred to as LXRβ-GFAP knockout mice) to cause anxiety-like behavior in adult mice.
The amygdala, mPFC, hypothalamus, hippocampus and other brain areas are the key brain areas that regulate anxiety, but in LXRβ-GFAP knockout mice, only the expression of LXRβ in the mPFC brain area is reduced.
LXRβ-GFAP knockout mice synapse proteins change excitatory/inhibitory synaptic disorders are the key mechanism of anxiety.
They found that the expression of excitatory synapse protein in the brain region of mPFC in LXRβ-GFAP knockout mice was significantly increased, but the inhibitory synapse protein did not change.
More surprisingly, this up-regulation of excitatory synaptic proteins only occurs in the 5th layer of the mPFC brain area.
Electrophysiological experiments have shown that the spontaneous inhibitory postsynaptic currents of neurons in the 5th layer of vertebral bodies have not changed, but spontaneously The excitatory postsynaptic current increases.
This indicates that the region's excitability/inhibitory imbalance is more biased towards excitability.
Virus strategy specifically knocks down LXRβ on astrocytes.
Researchers injected AAV-gfaABC1d-Cre virus into the mPFC region of LXRβ-floxp mice and were able to specifically knock out LXRβ on astrocytes.
Open field experiments, Elevated experiments and light-dark shuttle box experiments show that specific knockout of LXRβ can cause anxiety-like behaviors, and the spontaneous excitatory postsynaptic currents of vertebral neurons are also enhanced.
After being released into the synaptic cleft, the excitatory neurotransmitter glutamate is rapidly absorbed by GLT-1.
However, the expression of GLT-1 protein in mPFC brain regions of LXRβ-GFAP knockout mice and virus knockdown LXRβ mice was reduced.
After intraperitoneal injection of CEF can promote the expression of GLT-1 protein while reducing the spontaneous excitatory postsynaptic current, improving anxiety-like behavior.
Professor Fan Xiaotang’s research group focused on the key scientific issue in developmental biology "the pattern and mechanism of lamellar structure formation", focusing on the development and formation of estrogen receptor β (ERβ) and liver X receptor β (LXRβ) in the brain lamellar structure The role and mechanism of nuclear receptors, as well as the developmental regulatory mechanism of nuclear receptors in neuropsychological abnormalities and neuropsychiatric diseases.
In May 2018, Fan Xiaotang published an article in PNAS and found that after knocking out LXRβ, the formation of progenitor cells in the hippocampal DG area was abnormal and neurogenesis was reduced, causing autism-like behavior disorder.
[References] 1.
https://doi.
org/10.
1038/s41380-021-01139-5 The pictures in the article are all from the references.
If you need to download the original text, you can click on the Baidu web disk link: https://pan.
baidu.
com/ s/1dCtf4pltXiJj7DR1fcgXAw Extraction code: 9mif
