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Click on the blue word to focus on our central nervous system extracellular matrix components that provide structural support for neurons and regulate neuronal excitability and synaptic plastici.
Perineural networks (PNNs) are the main components of the extracellular matrix, mainly composed of hyaluronic acid, chondroitin sulfate proteoglycans,e.
PNNs in the cortex selectively encapsulate fast-spiking parvalbumin-positive inhibitory interneurons in the soma and proximal dendrites, regulating neural plastici.
On May 26, 2022, Science magazine published an article online by Arkady Khoutorsky's research team from McGill University in Canada in the form of a first release, finding that peripheral nerve injury caused a large number of PNNs in the spinal cord to degrade and cause pain behavior, which is mediated by microgl.
guid.
Wisteria agglutinin (WFA) selectively binds to the glycosaminoglycan chain (GAG) of PNN glycoprotei.
PNNs can be fluorescently labeled by WFA and aggrec.
Figure 1: Inhibitory synaptic structures are located in PN.
Immunofluorescence experiments found that PNNs were mainly surrounded by neurons in the spinal dorsal horn, and inhibitory presynaptic structures were located in PN.
PNNs are mainly distributed in the I slab, sparsely distributed in the III slab, and almost absent in the II sl.
Injecting retrograde gold particles into the lateral parabrachial nucleus found that PNNs in the I lamella selectively surrounded the spinal cord-parabrachial nucleus projection neurons, hereinafter referred to as the PNNs around the I lamellar projection neuro.
Activation of positive projection neurons in layer I PNNs was induced by mechanical or thermal noxious stimuli, suggesting that these neurons are involved in encoding pain-related informati.
Figure 2: Microglia phagocytosed PNNs after peripheral nerve injury 3 days after the pain behavior was the most obvious, at this time, the WFA-labeled PNNs in the I lamella were greatly reduced, and the levels remained low at 1 and 2 weeks after injury, but aggrecan-labeled PNNs were significantly reduc.
PNNs are not affect.
Immunofluorescence experiments found that the majority of microglia (61%) had co-labeling of WFA-labeled PNNs and lysosomes in the cells on the 3rd day after inju.
At the 1st and 2nd week after injury, the microglia phagocytosed PNNs The proportion of cytoplasmic cells was significantly reduc.
Peripheral nerve injury did not cause mechanical pain sensation nor degradation of PNNs after specific clearance of microglia in mice by the to.
There was also no significant decrease in PNNs around neurons in lamina I on day 3 after inju.
The chemokine receptor CX3CR1 mediates the activation and phagocytic activity of microgl.
The researchers found that the phagocytic activity of microglia was attenuated in CX3CR1 knockout mi.
CX3CR1-knockout mice did not show extensive degradation of PNNs around lamina I neurons after nerve inju.
These results suggest that microglia mediate the degradation of PNNs after peripheral nerve inju.
Normal mice showed reactions such as paw licking and jumping in the hot plate experime.
After the virus-binding aggrecan-cre mice specifically knocked out the PNNs around the projection neurons of the I lamella, the delay time of the above reactions was shortened, showing hypersensitivity to he.
allergic reacti.
Chondroitinase sulfate (ChABC) is a bacterial lyase that cleaves GAGs in PN.
Specific degradation of lamellar I projection neuron GAGs by a viral strategy induces spontaneous pain and induces thermal hypersensitivi.
I-lamellar PNNs-positive projection neurons receive more inhibitory input than excitatory inp.
Minimal inhibitory postsynaptic currents in neurons surrounding PNNs were reduced after CAG knockdown, manifesting as disinhibiti.
Collectively, this paper reveals that there is a class of neurons projecting to the lateral parabrachial nucleus in the lamina I of the spinal dorsal horn that is selectively encapsulated by PNNs, and engulfs a large number of PNNs after microglia activation after nerve injury, causing pain rea.
Click to download the original text: 0526-science-Microglia-mediated degradation of perineuronal nets promotes pa.
pdf
Perineural networks (PNNs) are the main components of the extracellular matrix, mainly composed of hyaluronic acid, chondroitin sulfate proteoglycans,e.
PNNs in the cortex selectively encapsulate fast-spiking parvalbumin-positive inhibitory interneurons in the soma and proximal dendrites, regulating neural plastici.
On May 26, 2022, Science magazine published an article online by Arkady Khoutorsky's research team from McGill University in Canada in the form of a first release, finding that peripheral nerve injury caused a large number of PNNs in the spinal cord to degrade and cause pain behavior, which is mediated by microgl.
guid.
Wisteria agglutinin (WFA) selectively binds to the glycosaminoglycan chain (GAG) of PNN glycoprotei.
PNNs can be fluorescently labeled by WFA and aggrec.
Figure 1: Inhibitory synaptic structures are located in PN.
Immunofluorescence experiments found that PNNs were mainly surrounded by neurons in the spinal dorsal horn, and inhibitory presynaptic structures were located in PN.
PNNs are mainly distributed in the I slab, sparsely distributed in the III slab, and almost absent in the II sl.
Injecting retrograde gold particles into the lateral parabrachial nucleus found that PNNs in the I lamella selectively surrounded the spinal cord-parabrachial nucleus projection neurons, hereinafter referred to as the PNNs around the I lamellar projection neuro.
Activation of positive projection neurons in layer I PNNs was induced by mechanical or thermal noxious stimuli, suggesting that these neurons are involved in encoding pain-related informati.
Figure 2: Microglia phagocytosed PNNs after peripheral nerve injury 3 days after the pain behavior was the most obvious, at this time, the WFA-labeled PNNs in the I lamella were greatly reduced, and the levels remained low at 1 and 2 weeks after injury, but aggrecan-labeled PNNs were significantly reduc.
PNNs are not affect.
Immunofluorescence experiments found that the majority of microglia (61%) had co-labeling of WFA-labeled PNNs and lysosomes in the cells on the 3rd day after inju.
At the 1st and 2nd week after injury, the microglia phagocytosed PNNs The proportion of cytoplasmic cells was significantly reduc.
Peripheral nerve injury did not cause mechanical pain sensation nor degradation of PNNs after specific clearance of microglia in mice by the to.
There was also no significant decrease in PNNs around neurons in lamina I on day 3 after inju.
The chemokine receptor CX3CR1 mediates the activation and phagocytic activity of microgl.
The researchers found that the phagocytic activity of microglia was attenuated in CX3CR1 knockout mi.
CX3CR1-knockout mice did not show extensive degradation of PNNs around lamina I neurons after nerve inju.
These results suggest that microglia mediate the degradation of PNNs after peripheral nerve inju.
Normal mice showed reactions such as paw licking and jumping in the hot plate experime.
After the virus-binding aggrecan-cre mice specifically knocked out the PNNs around the projection neurons of the I lamella, the delay time of the above reactions was shortened, showing hypersensitivity to he.
allergic reacti.
Chondroitinase sulfate (ChABC) is a bacterial lyase that cleaves GAGs in PN.
Specific degradation of lamellar I projection neuron GAGs by a viral strategy induces spontaneous pain and induces thermal hypersensitivi.
I-lamellar PNNs-positive projection neurons receive more inhibitory input than excitatory inp.
Minimal inhibitory postsynaptic currents in neurons surrounding PNNs were reduced after CAG knockdown, manifesting as disinhibiti.
Collectively, this paper reveals that there is a class of neurons projecting to the lateral parabrachial nucleus in the lamina I of the spinal dorsal horn that is selectively encapsulated by PNNs, and engulfs a large number of PNNs after microglia activation after nerve injury, causing pain rea.
Click to download the original text: 0526-science-Microglia-mediated degradation of perineuronal nets promotes pa.
