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Wenjing Luo
Fourth Military Medical University: Air Force Medical University
Corresponding Author
ORCiD: https://orcid.org/0000-0003-4826-3961
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Hypobaric hypoxia (HH) is a typical characteristic of high altitude environment and causes a spectrum of pathophysiological effects, including headaches, gliovascular dysfunction and cognitive slowing. Here, we sought to understand the mechanisms underlying cognitive deficits under HH exposure. Our results showed that HH exposure impaired cognitive function and suppressed dendritic spine density accompanied with increased neck length in both basal and apical hippocampal CA1 region neurons. The expression of PSD95, a critical synaptic scaffolding molecule, is down-regulated by hypoxia exposure and post-transcriptionally controlled by cold-inducible RNA-binding protein (Cirbp) through 3’-UTR region binding. PSD95 expressing alleviates hypoxia-induced neuron dendritic spine plasticity abnormality and memory impairment. Moreover, overexpressed Cirbp in hippocampus rescues hypoxia-induced loss of PSD95 and attenuates hypoxia-induced dendritic spine injury and cognitive outcomes. Thus, our findings reveal a novel mechanism where Cirbp-PSD-95 axis appears to play a key role in hypoxia-induced cognitive abilities impairment in brain.
Keywords
Hypoxia, Cognitive impairment, Dendritic spine morphology, cold-inducible RNA - binding protein, PSD95
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View the published article at Molecular Brain.
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Posted 25 Nov, 2020
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Review #2 received
Received 27 Jan, 2021
Editorial decision: Major revision
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Reviewer #2 agreed
On 12 Jan, 2021
Review #1 received
Received 07 Dec, 2020
Reviewer #1 agreed
On 22 Nov, 2020
Reviewers invited
Invitations sent on 20 Nov, 2020
Editor assigned
On 17 Nov, 2020
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On 17 Nov, 2020
Editor invited
On 17 Nov, 2020
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Subject Areas
Cellular & Molecular Neuroscience
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A new preprint design is coming!
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See the published version of this preprint at Molecular Brain.
This is a preprint, a preliminary version of a manuscript that has not completed peer review at a journal. Research Square does not conduct peer review prior to posting preprints. The posting of a preprint on this server should not be interpreted as an endorsement of its validity or suitability for dissemination as established information or for guiding clinical practice.
Learn more about In Review
Research
Wenjing Luo
Fourth Military Medical University: Air Force Medical University
Corresponding Author
ORCiD: https://orcid.org/0000-0003-4826-3961
Badges
Prescreen
This manuscript passed our Prescreen assessment
Complete author information
Appropriate declaration statements
Potential risks to human health
Prescreen
Peer Review Timeline
CURRENT STATUS: Published
View the published article at Molecular Brain.
Version 1
Posted 25 Nov, 2020
No community comments so far
Review #2 received
Received 27 Jan, 2021
Editorial decision: Major revision
On 27 Jan, 2021
Reviewer #2 agreed
On 12 Jan, 2021
Review #1 received
Received 07 Dec, 2020
Reviewer #1 agreed
On 22 Nov, 2020
Reviewers invited
Invitations sent on 20 Nov, 2020
Editor assigned
On 17 Nov, 2020
Submission checks complete
On 17 Nov, 2020
Editor invited
On 17 Nov, 2020
First submitted
On 14 Nov, 2020
Metrics
Comments: 0
PDF Downloads: ...
HTML Views: ...
Subject Areas
Cellular & Molecular Neuroscience
License:
This work is licensed under a CC BY 4.0 License. Read Full License
View the published article at Molecular Brain.
Hypobaric hypoxia (HH) is a typical characteristic of high altitude environment and causes a spectrum of pathophysiological effects, including headaches, gliovascular dysfunction and cognitive slowing. Here, we sought to understand the mechanisms underlying cognitive deficits under HH exposure. Our results showed that HH exposure impaired cognitive function and suppressed dendritic spine density accompanied with increased neck length in both basal and apical hippocampal CA1 region neurons. The expression of PSD95, a critical synaptic scaffolding molecule, is down-regulated by hypoxia exposure and post-transcriptionally controlled by cold-inducible RNA-binding protein (Cirbp) through 3’-UTR region binding. PSD95 expressing alleviates hypoxia-induced neuron dendritic spine plasticity abnormality and memory impairment. Moreover, overexpressed Cirbp in hippocampus rescues hypoxia-induced loss of PSD95 and attenuates hypoxia-induced dendritic spine injury and cognitive outcomes. Thus, our findings reveal a novel mechanism where Cirbp-PSD-95 axis appears to play a key role in hypoxia-induced cognitive abilities impairment in brain.
Figure 1
Figure 2
Figure 3
Figure 4
Figure 5
Figure 6
The full text of this article is available to read as a PDF.
This is a list of supplementary files associated with this preprint. Click to download.
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