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Click on the blue word to pay attention to our serious traumatic events will produce persistent, negative memories in the brain, and then may produce long-term fear and stress-related disease states, such as post-traumatic stress disorder (PTSD).
The prevalence of PTSD in the general population is 7%, but after severe traumatic stress, the prevalence rate is as high as 28%.
The expression of intrusive memory that is difficult to control and frustrating is the main feature of post-traumatic stress disorder (PTSD).
Attempts to suppress or avoid traumatic memories sometimes abnormally increase the expression of intrusive memories.
The most effective way to treat PTSD is exposure therapy.
Scientists used rodents' fear memory dissipation model to study exposure therapy and discovered the key neural circuit mechanism of fear memory dissipation.
On May 17, 2021, the Johannes Gräff research team of the Faculty of Life Sciences at the Federal Institute of Technology in Lausanne published an article in the journal Nature Neuroscience, revealing the neural circuit mechanism that regulates the dissipation of long-term fear memory: IL→NRe→BLA.
The inferior marginal area (IL) of the prefrontal cortex and the basolateral amygdala (BLA) are the key brain areas for the dissipation of conditioned fear memories.
The researchers injected the retrograde tracer virus AAV2r-CAG::Tom into the BLA area and performed the dissipating training of short-term fear memory (1 day) and long-term fear memory (30 days).
Neural circuits activated in the recent fear memory dissipating experiment In the recent fear memory dissipating experiment, a large number of neurons projecting from IL to BLA were activated, but the neurons projecting to BLA from the central nucleus of the thalamus (NRe) and from IL to NRe did not appear.
Mass activation.Neural circuits activated by the long-term fear memory dissipating experiment In the long-term fear memory dissipating experiment, although the neurons that project IL to BLA are not activated in large numbers, the brain area of NRe serves as a good "bridge" function, IL projection A large number of neurons that project to BLA from NRe and NRe are activated, which indicates that the IL→NRe→BLA neural circuit mediates the dissipation of long-term fear memory.
The fiber-optic calcium imaging system records the fear memory response at different stages.
NRe plays an important role in the consolidation of long-term fear memory.
After injecting the calcium ion indicator AAV1-CamKII::GCaMP6f, which can be expressed in excitatory neurons, into the NRe brain area, it was found that the changes of calcium ion in the NRe brain area appeared before the rigid response during memory extraction withdrawal and disappearance withdrawal.
The lead time is about 500 milliseconds and the duration is 200 milliseconds; however, this change does not appear in normal mice.
It shows that the NRe brain area is indeed related to the fear response.
They injected the chemosuppressive genetic virus AVV8-hSyn::hM4Di-mCherry into the brain area of NRe to enhance the expression process of long-term fear memory in mice.
Activation of neurons in this brain area can reduce the expression of fear memory during dissipative training.
This shows that the NRe brain area regulates the dissipating process of long-term fear memory in both directions.
The closed-loop light activation of the NRe→BLA neural circuit can reduce the expression of fear memory in mice during the dissipating process of long-term fear memory.
Glutamate-induced changes in synaptic plasticity are generally mediated by AMPA and NMDA receptors.
Researchers found that the ratio of AMPA/NMDA increased significantly during the process of long-term fear memory dissipating, and the increase in the ratio could be suppressed by activating the above-mentioned neural circuits.
This indicates that the dissipation of long-term fear memory specifically enhances the synaptic input of NRe→BLA.
In general, this article found that although the IL→BLA neural circuit is not directly involved in regulating the dissipation of long-term fear memory, it is indirectly involved in the above dissipation process through the "middleman" NRe.
[References] 1.
https://doi.
org/10.
1038/s41593-021-00856-y, the pictures in the text are all from the references
The prevalence of PTSD in the general population is 7%, but after severe traumatic stress, the prevalence rate is as high as 28%.
The expression of intrusive memory that is difficult to control and frustrating is the main feature of post-traumatic stress disorder (PTSD).
Attempts to suppress or avoid traumatic memories sometimes abnormally increase the expression of intrusive memories.
The most effective way to treat PTSD is exposure therapy.
Scientists used rodents' fear memory dissipation model to study exposure therapy and discovered the key neural circuit mechanism of fear memory dissipation.
On May 17, 2021, the Johannes Gräff research team of the Faculty of Life Sciences at the Federal Institute of Technology in Lausanne published an article in the journal Nature Neuroscience, revealing the neural circuit mechanism that regulates the dissipation of long-term fear memory: IL→NRe→BLA.
The inferior marginal area (IL) of the prefrontal cortex and the basolateral amygdala (BLA) are the key brain areas for the dissipation of conditioned fear memories.
The researchers injected the retrograde tracer virus AAV2r-CAG::Tom into the BLA area and performed the dissipating training of short-term fear memory (1 day) and long-term fear memory (30 days).
Neural circuits activated in the recent fear memory dissipating experiment In the recent fear memory dissipating experiment, a large number of neurons projecting from IL to BLA were activated, but the neurons projecting to BLA from the central nucleus of the thalamus (NRe) and from IL to NRe did not appear.
Mass activation.Neural circuits activated by the long-term fear memory dissipating experiment In the long-term fear memory dissipating experiment, although the neurons that project IL to BLA are not activated in large numbers, the brain area of NRe serves as a good "bridge" function, IL projection A large number of neurons that project to BLA from NRe and NRe are activated, which indicates that the IL→NRe→BLA neural circuit mediates the dissipation of long-term fear memory.
The fiber-optic calcium imaging system records the fear memory response at different stages.
NRe plays an important role in the consolidation of long-term fear memory.
After injecting the calcium ion indicator AAV1-CamKII::GCaMP6f, which can be expressed in excitatory neurons, into the NRe brain area, it was found that the changes of calcium ion in the NRe brain area appeared before the rigid response during memory extraction withdrawal and disappearance withdrawal.
The lead time is about 500 milliseconds and the duration is 200 milliseconds; however, this change does not appear in normal mice.
It shows that the NRe brain area is indeed related to the fear response.
They injected the chemosuppressive genetic virus AVV8-hSyn::hM4Di-mCherry into the brain area of NRe to enhance the expression process of long-term fear memory in mice.
Activation of neurons in this brain area can reduce the expression of fear memory during dissipative training.
This shows that the NRe brain area regulates the dissipating process of long-term fear memory in both directions.
The closed-loop light activation of the NRe→BLA neural circuit can reduce the expression of fear memory in mice during the dissipating process of long-term fear memory.
Glutamate-induced changes in synaptic plasticity are generally mediated by AMPA and NMDA receptors.
Researchers found that the ratio of AMPA/NMDA increased significantly during the process of long-term fear memory dissipating, and the increase in the ratio could be suppressed by activating the above-mentioned neural circuits.
This indicates that the dissipation of long-term fear memory specifically enhances the synaptic input of NRe→BLA.
In general, this article found that although the IL→BLA neural circuit is not directly involved in regulating the dissipation of long-term fear memory, it is indirectly involved in the above dissipation process through the "middleman" NRe.
[References] 1.
https://doi.
org/10.
1038/s41593-021-00856-y, the pictures in the text are all from the references
