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Click on the blue letters to pay attention to the ultrastructure of our synapses as neurons, which is an important "platform" for neurons to function
.
Although synapses are small, they also have surprising molecular and functional heterogeneity, especially excitatory and inhibitory synapses
.
Synaptic excitability/inhibitory imbalance is an important pathogenesis of autism, depression and other psychiatric diseases
.
Microglia, as the main immune cells in the brain, can reshape synapses: clear more weak synapses during development to form correct neural circuits, and in pathological conditions, microglia can swallow more Synapses cause cognitive dysfunction
.
On July 8, 2021, the Gord Fishell research team of Harvard Medical School's Blavatnik Institute of Neuroscience revealed the mechanism by which developing microglia specifically shape inhibitory synapses
.
The mouse somatosensory (S1) cortex expresses the most abundant microalbumin neurons in the brain region.
The researchers chose this brain region to study the relationship between microglia and inhibitory synapses
.
The removal of microglia during the developmental period causes an increase in the number of inhibitory synapses.
On the 4th day after birth (P4), mice were injected with the colony stimulating factor receptor inhibitor PLX5622, and the inhibitory synapses on the excitatory neurons in the S1 area on P15 The number has increased significantly
.
Electrophysiological experiments have found that the activation of PV neurons by light causes an increase in inhibitory postsynaptic currents
.
It was further found that the number of inhibitory synapses did not change significantly until the 12th day after P0 eliminated microglia
.
The elimination of microglia at the 3rd or 4th week after birth will not cause the change in the number of inhibitory synapses
.
These results indicate that microglia are more pruning existing synaptic connections rather than promoting the formation of these functional connections
.
Of course, the remodeling of excitatory or inhibitory synapses by microglia is affected by rain and dew: after the elimination of microglia at P0, PVrgic neurons cause an increase in excitatory postsynaptic currents on the 15th day
.
This indicates that microglia regulate excitatory and inhibitory synapses during development
.
Phagocytosis-inhibiting synapses of developing microglia.
Researchers used CX3CR1 tool mice and AAV virus vector tools to label microglia cells to specific synaptic ends of PV-ergic neurons, and found that under normal conditions P12 microglia Cell phagocytosis of PV can reach the end of synapse, peaking during P15-P17, and gradually decreasing during P30
.
During P15, the complement protein C1Q accumulates at the ends of PV-ergic synapses
.
The number of inhibitory synapses increases during P15 after C1Q is knocked out, and the inhibitory postsynaptic current increases, which can simulate the changes in the morphology and function of inhibitory synapses after knocking out microglia
.
Microglia express GABAB receptor subunits Gabbr1 and Gabbr2 as inhibitory neurotransmitters.
GABA can regulate stem cell proliferation, migration, synapseogenesis, synaptic pruning and astrocyte activity and other developmental activities
.
Previous studies have shown that microglia express GABAB receptors
.
Researchers found through in situ hybridization experiments that microglia express GABAB receptor subunits Gabbr1 and Gabbr2
.
Three-dimensional reconstruction experiments found that PV can be more phagocytosed by Gabbr2-expressing microglia
.
After specifically knocking out the GABAB receptor on microglia, the phagocytic inhibitory synapse of microglia is reduced, and it has no effect on excitatory synapses
.
This indicates that microglia can selectively trim inhibitory synapses through their GABAB receptors
.
In behavioral studies, specifically knocking out GABAB receptors on microglia, P30 mice showed reduced activity, but they were overactive in adulthood (P60 mice).
This is attention deficit hyperactivity disorder (ADHD).
) Core symptoms
.
In summary, this article found that microglia expressing GABAB receptors can selectively prune inhibitory synapses, if this function is impaired during development and causes adult ADHD
.
[References] 1.
https://doi.
org/10.
1016/j.
neuron.
2021.
06.
012 The pictures in the article are all from the reference original download link: https://pan.
baidu.
com/s/1BecgnAn8vLwCCt6p2Dj2gQ Extraction code: te6y
.
Although synapses are small, they also have surprising molecular and functional heterogeneity, especially excitatory and inhibitory synapses
.
Synaptic excitability/inhibitory imbalance is an important pathogenesis of autism, depression and other psychiatric diseases
.
Microglia, as the main immune cells in the brain, can reshape synapses: clear more weak synapses during development to form correct neural circuits, and in pathological conditions, microglia can swallow more Synapses cause cognitive dysfunction
.
On July 8, 2021, the Gord Fishell research team of Harvard Medical School's Blavatnik Institute of Neuroscience revealed the mechanism by which developing microglia specifically shape inhibitory synapses
.
The mouse somatosensory (S1) cortex expresses the most abundant microalbumin neurons in the brain region.
The researchers chose this brain region to study the relationship between microglia and inhibitory synapses
.
The removal of microglia during the developmental period causes an increase in the number of inhibitory synapses.
On the 4th day after birth (P4), mice were injected with the colony stimulating factor receptor inhibitor PLX5622, and the inhibitory synapses on the excitatory neurons in the S1 area on P15 The number has increased significantly
.
Electrophysiological experiments have found that the activation of PV neurons by light causes an increase in inhibitory postsynaptic currents
.
It was further found that the number of inhibitory synapses did not change significantly until the 12th day after P0 eliminated microglia
.
The elimination of microglia at the 3rd or 4th week after birth will not cause the change in the number of inhibitory synapses
.
These results indicate that microglia are more pruning existing synaptic connections rather than promoting the formation of these functional connections
.
Of course, the remodeling of excitatory or inhibitory synapses by microglia is affected by rain and dew: after the elimination of microglia at P0, PVrgic neurons cause an increase in excitatory postsynaptic currents on the 15th day
.
This indicates that microglia regulate excitatory and inhibitory synapses during development
.
Phagocytosis-inhibiting synapses of developing microglia.
Researchers used CX3CR1 tool mice and AAV virus vector tools to label microglia cells to specific synaptic ends of PV-ergic neurons, and found that under normal conditions P12 microglia Cell phagocytosis of PV can reach the end of synapse, peaking during P15-P17, and gradually decreasing during P30
.
During P15, the complement protein C1Q accumulates at the ends of PV-ergic synapses
.
The number of inhibitory synapses increases during P15 after C1Q is knocked out, and the inhibitory postsynaptic current increases, which can simulate the changes in the morphology and function of inhibitory synapses after knocking out microglia
.
Microglia express GABAB receptor subunits Gabbr1 and Gabbr2 as inhibitory neurotransmitters.
GABA can regulate stem cell proliferation, migration, synapseogenesis, synaptic pruning and astrocyte activity and other developmental activities
.
Previous studies have shown that microglia express GABAB receptors
.
Researchers found through in situ hybridization experiments that microglia express GABAB receptor subunits Gabbr1 and Gabbr2
.
Three-dimensional reconstruction experiments found that PV can be more phagocytosed by Gabbr2-expressing microglia
.
After specifically knocking out the GABAB receptor on microglia, the phagocytic inhibitory synapse of microglia is reduced, and it has no effect on excitatory synapses
.
This indicates that microglia can selectively trim inhibitory synapses through their GABAB receptors
.
In behavioral studies, specifically knocking out GABAB receptors on microglia, P30 mice showed reduced activity, but they were overactive in adulthood (P60 mice).
This is attention deficit hyperactivity disorder (ADHD).
) Core symptoms
.
In summary, this article found that microglia expressing GABAB receptors can selectively prune inhibitory synapses, if this function is impaired during development and causes adult ADHD
.
[References] 1.
https://doi.
org/10.
1016/j.
neuron.
2021.
06.
012 The pictures in the article are all from the reference original download link: https://pan.
baidu.
com/s/1BecgnAn8vLwCCt6p2Dj2gQ Extraction code: te6y
