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In modern society, with the rapid development of social economy, people are facing increasing challenges and pressures in life and work
.
As we all know, excessive or long-term stress exposure is closely related to the onset of a series of physical and mental diseases such as anxiety and depression; and the frequent occurrence of mental diseases such as anxiety has become a global public health problem that seriously threatens people's health
.
Recent epidemiological surveys show that in China, the lifetime prevalence rate of anxiety disorders is as high as 7.
6%, and the annual prevalence rate is 5.
0%, but the current prevention and treatment of anxiety disorders is still far from satisfactory
.
Among them, the limited cognition of the pathogenesis of anxiety disorders is an important factor restricting the development of disease prevention and treatment strategies
.
The amygdala is the core brain area where the brain expresses and regulates anxiety and other emotions
.
In the resting state, the amygdala presents a highly inhibited state; while under chronic stress, the highly inhibited state of the amygdala is released (de-inhibited), causing excessive neuronal excitement
.
Amygdala disinhibition is considered to be an important neurobiological basis for affective disorders caused by chronic stress
.
A large number of studies have shown that the inhibitory signal mediated by the inhibitory neurotransmitter-GABA is widely involved in the excessive activation of amygdala neurons caused by chronic stress
.
GABA mainly exerts fast and slow inhibitory effects by activating ionized GABAAR and metabolized GABABR, respectively
.
The activation of GABAAR located in the synapse produces a temporal inhibitory current, while the activation of GABAAR located outside the synapse produces a tonic inhibitory current
.
Recently, the research group of Professor Pan Bingxing from the Institute of Life Sciences of Nanchang University (Dr.
Xia Qin is the first author of the paper, Professor Pan Bingxing and Associate Researcher Zhang Wenhua are the co-corresponding authors of the paper) published an online publication titled "GABAA(δ) receptor hypofunction" on Science Bulletin.
in the amygdala-hippocampal circuit underlies stress-induced anxiety" research paper reported that chronic stress down-regulates a type of GABAA receptor (GABAA(δ The expression and function of )R) eventually cause anxiety disorders, and the related neural circuit mechanisms are deeply analyzed
.
In this study, they established a chronic social frustration stress (CSDS) model to observe the effect of chronic stress on the inhibitory currents of different types of projection neurons in the basolateral amygdala (BLA)
.
It was found that CSDS down-regulated the tonic currents projected to the ventral hippocampal (BLA→vHPC) neurons in the BLA, but up-regulated the tonic currents projected to the anterior dorsal stria terminalis bed nucleus (BLA→adBNST) neurons
.
In view of the important regulatory effect of tonic inhibitory current on neuronal activity, they further found that CSDS eliminated and enhanced the GABAergic inhibitory effects of BLA→vHPC and BLA→adBNST neurons, respectively
.
The researchers further explored the role of CSDS in the differential regulation of BLA→vHPC and BLA→adBNST neuronal tension inhibitory currents in increasing anxiety-like behaviors in mice
.
The results showed that the increase of anxiety-like behavior in mice caused by CSDS was significantly correlated with the down-regulation of BLA→vHPC neuron tonic current, but there was no significant correlation with its up-regulation of BLA→adBNST neuron tonic current
.
In order to clarify the receptor mechanism of CSDS differential regulation of BLA→vHPC and BLA→adBNST neuronal tonic inhibitory currents, they used single-cell quantitative PCR detection, pharmacology, and gene knockout methods, and found that GABAA(δ)R mediates An important medium for CSDS differential regulation
.
CSDS significantly down-regulates the expression of GABAA(δ)R in BLA→vHPC neurons and the tonic inhibitory current mediated by it; on the contrary, it up-regulates the expression of GABAA(δ)R and the tonic inhibitory current in BLA→adBNST neurons Effect
.
In terms of pathological function, the down-regulation of the tonic inhibitory current on BLA→vHPC neurons participates in the excessive anxiety caused by chronic stress, but the change of the tonic inhibitory current on BLA→adBNST neurons does not participate in the above process
.
In conclusion, this study shows that chronic stress can selectively reduce the GABAA(δ)R-mediated tonic inhibitory current in BLA→vHPC neurons, thereby down-regulating the ability of GABA to inhibit the activity of these neurons, causing mice to produce Excessive anxiety-like behavior
.
This study reveals the differential regulation of chronic stress on the tonic inhibitory currents of different neurons in the amygdala, and clarifies the specific receptors and molecular mechanisms, which are expected to provide important clues for the precise intervention of stress-related diseases
.
Original link ▼https://
.
As we all know, excessive or long-term stress exposure is closely related to the onset of a series of physical and mental diseases such as anxiety and depression; and the frequent occurrence of mental diseases such as anxiety has become a global public health problem that seriously threatens people's health
.
Recent epidemiological surveys show that in China, the lifetime prevalence rate of anxiety disorders is as high as 7.
6%, and the annual prevalence rate is 5.
0%, but the current prevention and treatment of anxiety disorders is still far from satisfactory
.
Among them, the limited cognition of the pathogenesis of anxiety disorders is an important factor restricting the development of disease prevention and treatment strategies
.
The amygdala is the core brain area where the brain expresses and regulates anxiety and other emotions
.
In the resting state, the amygdala presents a highly inhibited state; while under chronic stress, the highly inhibited state of the amygdala is released (de-inhibited), causing excessive neuronal excitement
.
Amygdala disinhibition is considered to be an important neurobiological basis for affective disorders caused by chronic stress
.
A large number of studies have shown that the inhibitory signal mediated by the inhibitory neurotransmitter-GABA is widely involved in the excessive activation of amygdala neurons caused by chronic stress
.
GABA mainly exerts fast and slow inhibitory effects by activating ionized GABAAR and metabolized GABABR, respectively
.
The activation of GABAAR located in the synapse produces a temporal inhibitory current, while the activation of GABAAR located outside the synapse produces a tonic inhibitory current
.
Recently, the research group of Professor Pan Bingxing from the Institute of Life Sciences of Nanchang University (Dr.
Xia Qin is the first author of the paper, Professor Pan Bingxing and Associate Researcher Zhang Wenhua are the co-corresponding authors of the paper) published an online publication titled "GABAA(δ) receptor hypofunction" on Science Bulletin.
in the amygdala-hippocampal circuit underlies stress-induced anxiety" research paper reported that chronic stress down-regulates a type of GABAA receptor (GABAA(δ The expression and function of )R) eventually cause anxiety disorders, and the related neural circuit mechanisms are deeply analyzed
.
In this study, they established a chronic social frustration stress (CSDS) model to observe the effect of chronic stress on the inhibitory currents of different types of projection neurons in the basolateral amygdala (BLA)
.
It was found that CSDS down-regulated the tonic currents projected to the ventral hippocampal (BLA→vHPC) neurons in the BLA, but up-regulated the tonic currents projected to the anterior dorsal stria terminalis bed nucleus (BLA→adBNST) neurons
.
In view of the important regulatory effect of tonic inhibitory current on neuronal activity, they further found that CSDS eliminated and enhanced the GABAergic inhibitory effects of BLA→vHPC and BLA→adBNST neurons, respectively
.
The researchers further explored the role of CSDS in the differential regulation of BLA→vHPC and BLA→adBNST neuronal tension inhibitory currents in increasing anxiety-like behaviors in mice
.
The results showed that the increase of anxiety-like behavior in mice caused by CSDS was significantly correlated with the down-regulation of BLA→vHPC neuron tonic current, but there was no significant correlation with its up-regulation of BLA→adBNST neuron tonic current
.
In order to clarify the receptor mechanism of CSDS differential regulation of BLA→vHPC and BLA→adBNST neuronal tonic inhibitory currents, they used single-cell quantitative PCR detection, pharmacology, and gene knockout methods, and found that GABAA(δ)R mediates An important medium for CSDS differential regulation
.
CSDS significantly down-regulates the expression of GABAA(δ)R in BLA→vHPC neurons and the tonic inhibitory current mediated by it; on the contrary, it up-regulates the expression of GABAA(δ)R and the tonic inhibitory current in BLA→adBNST neurons Effect
.
In terms of pathological function, the down-regulation of the tonic inhibitory current on BLA→vHPC neurons participates in the excessive anxiety caused by chronic stress, but the change of the tonic inhibitory current on BLA→adBNST neurons does not participate in the above process
.
In conclusion, this study shows that chronic stress can selectively reduce the GABAA(δ)R-mediated tonic inhibitory current in BLA→vHPC neurons, thereby down-regulating the ability of GABA to inhibit the activity of these neurons, causing mice to produce Excessive anxiety-like behavior
.
This study reveals the differential regulation of chronic stress on the tonic inhibitory currents of different neurons in the amygdala, and clarifies the specific receptors and molecular mechanisms, which are expected to provide important clues for the precise intervention of stress-related diseases
.
Original link ▼https://
