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Editor’s note iNature is China’s largest academic official account.
It is jointly created by the doctoral team of Tsinghua University, Harvard University, Chinese Academy of Sciences and other units.
The iNature Talent Official Account is now launched, focusing on talent recruitment, academic progress, scientific research information, interested parties can Long press or scan the QR code below to follow us
.
iNature memory persistence is the basic cognitive process that guides behavior, and it is believed that it mainly depends on neuronal and synaptic plasticity
.
Whether and how astrocytes promote memory persistence is largely unknown
.
On November 15, 2021, Chen Xiaowei, Army Medical University and Arthur Konnerth of Technical University of Munich, Germany, jointly published an online report entitled "Fear learning induces α7-nicotinic acetylcholine receptor-mediated astrocytic responsiveness that is required for memory persistence" in Nature Neuroscience.
Research paper, this study uses two-photon Ca2+ imaging in head-fixed mice and fiber photometry in free-moving mice, showing that sensory stimulation of aversion activates α7- in a subpopulation of astrocytes in the auditory cortex.
Nicotinic Acetylcholine Receptors (nAChRs)
.
This study demonstrates that fear learning leads to the de novo induction of sound-induced Ca2+ transients in these astrocytes
.
The reactivity of astrocytes lasted for several days with fear memory, and disappeared in animals that had experienced the extinction of learned freezing behavior
.
The conditional gene deletion of α7-nAChRs in astrocytes significantly impairs the persistence of fear memory
.
In conclusion, the study found that learning acquisition and α7-nAChR-dependent astrocyte reactivity are components of the basic cell matrix for memory persistence
.
Memory persistence or memory refers to the systematic process of storing information permanently in the brain and categorizing it so that it can be retrieved upon request
.
This basic cognitive process plays a central role in guiding behaviors that are vital to survival and is often impaired in neurological diseases such as Alzheimer's disease or traumatic brain injury
.
Previous studies have focused extensively on the role of neurons in memory persistence
.
It has been suggested that memory persistence involves the replay of neuronal activity patterns present in coding
.
In order to increase the possibility of a specific activity pattern reappearing later, memory persistence needs to be strengthened or weakened in synaptic connections within the collection of participating neurons
.
Therefore, any factor that can change the strength of synaptic connections in a particular neuron network may affect memory persistence
.
More and more experimental evidence shows that glial cells are important regulators of synaptic function and plasticity
.
Astrocytes are a major type of glial cells that respond to neuronal activity through intracellular Ca2+ transients, and then release glial transmitters to change synaptic connections
.
This mutual neuron-astrocytic interaction has led to the concept of "triple synapses," in which astrocytes are considered to be active participants in synaptic processing
.
Fear learning training can induce astrocytes to produce calcium signals (picture from Nature Neuroscience) Astrocytes express different types of neurotransmitter receptors, including noradrenergic, glutamatergic and cholinergic Receptor
.
Through these receptors, astrocytes in the central nervous system respond to various sensory stimuli, including smell, light, sound, touch, and pain
.
These astrocyte signals not only regulate synapse formation, transmission and plasticity, but also regulate the synchronization of neuronal group activity
.
Therefore, through the multi-scale regulation of neuronal activity during external sensory stimulation, astrocytes are in an ideal position to promote memory formation and persistence
.
In fact, astrocytes have been repeatedly shown to be involved in neuronal plasticity in vitro and in vivo
.
In addition, more and more studies have revealed the necessity of astrocytes for normal memory function in the body
.
These studies show that interference with astrocyte activity can lead to memory impairment
.
In addition, recent studies have shown that adding human astrocytes to the mouse brain or artificially activating astrocytes can lead to enhanced memory
.
However, in the process of information acquisition and storage, whether and how the astrocyte activity related to memory changes is unclear, because it recognizes functionally defined astrocytes in the body and monitors their behavior at different stages of learning Activities are difficult
.
Fear memories can remain intact throughout a lifetime
.
Recent studies have shown that astrocytes contribute to the initial stages of the acquisition and consolidation of fear memories
.
Artificial activation of astrocytes through chemical genetic manipulation in the CA1 region of the hippocampus can enhance the acquisition of fear memories, but may reduce the expression of fear in the inner subdivision of the central amygdala
.
In addition, in the auditory cortex, fear learning has been shown to involve neuronal plasticity and rely on the recruitment of α7-nAchR-mediated de-inhibitory neuronal circuit activation
.
However, it is not clear whether astrocytes in the auditory cortex are involved in the formation and persistence of fear memories
.
The study used two-photon Ca2+ imaging in head-fixed mice and fiber photometry in freely moving mice, showing that sensory stimulation of aversion activates α7-nicotinic acetylcholine in a subpopulation of astrocytes in the auditory cortex Receptors (nAChRs)
.
This study demonstrates that fear learning leads to the de novo induction of sound-induced Ca2+ transients in these astrocytes
.
The responsiveness of astrocytes lasted for several days with fear memory, and disappeared in animals that had experienced the extinction of learned freezing behavior
.
The conditional gene deletion of α7-nAChRs in astrocytes significantly impairs the persistence of fear memory
.
In conclusion, the study found that learning acquisition and α7-nAChR-dependent astrocyte reactivity are components of the basic cell matrix for memory persistence
.
The first author of this work is Zhang Kuan of the Army Military Medical University, and the last corresponding author is Chen Xiaowei of the Army Military Medical University.
The co-first and co-corresponding authors are Rita Förster and Arthur Konnerth of the Technical University of Munich, Germany
.
The cooperation team also includes: Liao Xiang Group of the Institute of Neuro-Intelligence, Chongqing University School of Medicine, Qin Song Group, School of Basic Medicine, Fudan University, Chen Tao Group, School of Basic Medicine, Air Force Military Medical University, Bruno Weber Group, Zurich Neuroscience Center, University of Zurich, Brain and Intelligence, Guangxi University Research centers, etc.
; this work was funded by the National Key Research and Development Program (Young Scientist Project), the National Natural Science Foundation of China, the China Scholarship Council, Chongqing Science and Technology Bureau, the European Research Council Fund, and the German Science Foundation
.
Reference message: https://
It is jointly created by the doctoral team of Tsinghua University, Harvard University, Chinese Academy of Sciences and other units.
The iNature Talent Official Account is now launched, focusing on talent recruitment, academic progress, scientific research information, interested parties can Long press or scan the QR code below to follow us
.
iNature memory persistence is the basic cognitive process that guides behavior, and it is believed that it mainly depends on neuronal and synaptic plasticity
.
Whether and how astrocytes promote memory persistence is largely unknown
.
On November 15, 2021, Chen Xiaowei, Army Medical University and Arthur Konnerth of Technical University of Munich, Germany, jointly published an online report entitled "Fear learning induces α7-nicotinic acetylcholine receptor-mediated astrocytic responsiveness that is required for memory persistence" in Nature Neuroscience.
Research paper, this study uses two-photon Ca2+ imaging in head-fixed mice and fiber photometry in free-moving mice, showing that sensory stimulation of aversion activates α7- in a subpopulation of astrocytes in the auditory cortex.
Nicotinic Acetylcholine Receptors (nAChRs)
.
This study demonstrates that fear learning leads to the de novo induction of sound-induced Ca2+ transients in these astrocytes
.
The reactivity of astrocytes lasted for several days with fear memory, and disappeared in animals that had experienced the extinction of learned freezing behavior
.
The conditional gene deletion of α7-nAChRs in astrocytes significantly impairs the persistence of fear memory
.
In conclusion, the study found that learning acquisition and α7-nAChR-dependent astrocyte reactivity are components of the basic cell matrix for memory persistence
.
Memory persistence or memory refers to the systematic process of storing information permanently in the brain and categorizing it so that it can be retrieved upon request
.
This basic cognitive process plays a central role in guiding behaviors that are vital to survival and is often impaired in neurological diseases such as Alzheimer's disease or traumatic brain injury
.
Previous studies have focused extensively on the role of neurons in memory persistence
.
It has been suggested that memory persistence involves the replay of neuronal activity patterns present in coding
.
In order to increase the possibility of a specific activity pattern reappearing later, memory persistence needs to be strengthened or weakened in synaptic connections within the collection of participating neurons
.
Therefore, any factor that can change the strength of synaptic connections in a particular neuron network may affect memory persistence
.
More and more experimental evidence shows that glial cells are important regulators of synaptic function and plasticity
.
Astrocytes are a major type of glial cells that respond to neuronal activity through intracellular Ca2+ transients, and then release glial transmitters to change synaptic connections
.
This mutual neuron-astrocytic interaction has led to the concept of "triple synapses," in which astrocytes are considered to be active participants in synaptic processing
.
Fear learning training can induce astrocytes to produce calcium signals (picture from Nature Neuroscience) Astrocytes express different types of neurotransmitter receptors, including noradrenergic, glutamatergic and cholinergic Receptor
.
Through these receptors, astrocytes in the central nervous system respond to various sensory stimuli, including smell, light, sound, touch, and pain
.
These astrocyte signals not only regulate synapse formation, transmission and plasticity, but also regulate the synchronization of neuronal group activity
.
Therefore, through the multi-scale regulation of neuronal activity during external sensory stimulation, astrocytes are in an ideal position to promote memory formation and persistence
.
In fact, astrocytes have been repeatedly shown to be involved in neuronal plasticity in vitro and in vivo
.
In addition, more and more studies have revealed the necessity of astrocytes for normal memory function in the body
.
These studies show that interference with astrocyte activity can lead to memory impairment
.
In addition, recent studies have shown that adding human astrocytes to the mouse brain or artificially activating astrocytes can lead to enhanced memory
.
However, in the process of information acquisition and storage, whether and how the astrocyte activity related to memory changes is unclear, because it recognizes functionally defined astrocytes in the body and monitors their behavior at different stages of learning Activities are difficult
.
Fear memories can remain intact throughout a lifetime
.
Recent studies have shown that astrocytes contribute to the initial stages of the acquisition and consolidation of fear memories
.
Artificial activation of astrocytes through chemical genetic manipulation in the CA1 region of the hippocampus can enhance the acquisition of fear memories, but may reduce the expression of fear in the inner subdivision of the central amygdala
.
In addition, in the auditory cortex, fear learning has been shown to involve neuronal plasticity and rely on the recruitment of α7-nAchR-mediated de-inhibitory neuronal circuit activation
.
However, it is not clear whether astrocytes in the auditory cortex are involved in the formation and persistence of fear memories
.
The study used two-photon Ca2+ imaging in head-fixed mice and fiber photometry in freely moving mice, showing that sensory stimulation of aversion activates α7-nicotinic acetylcholine in a subpopulation of astrocytes in the auditory cortex Receptors (nAChRs)
.
This study demonstrates that fear learning leads to the de novo induction of sound-induced Ca2+ transients in these astrocytes
.
The responsiveness of astrocytes lasted for several days with fear memory, and disappeared in animals that had experienced the extinction of learned freezing behavior
.
The conditional gene deletion of α7-nAChRs in astrocytes significantly impairs the persistence of fear memory
.
In conclusion, the study found that learning acquisition and α7-nAChR-dependent astrocyte reactivity are components of the basic cell matrix for memory persistence
.
The first author of this work is Zhang Kuan of the Army Military Medical University, and the last corresponding author is Chen Xiaowei of the Army Military Medical University.
The co-first and co-corresponding authors are Rita Förster and Arthur Konnerth of the Technical University of Munich, Germany
.
The cooperation team also includes: Liao Xiang Group of the Institute of Neuro-Intelligence, Chongqing University School of Medicine, Qin Song Group, School of Basic Medicine, Fudan University, Chen Tao Group, School of Basic Medicine, Air Force Military Medical University, Bruno Weber Group, Zurich Neuroscience Center, University of Zurich, Brain and Intelligence, Guangxi University Research centers, etc.
; this work was funded by the National Key Research and Development Program (Young Scientist Project), the National Natural Science Foundation of China, the China Scholarship Council, Chongqing Science and Technology Bureau, the European Research Council Fund, and the German Science Foundation
.
Reference message: https://
