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Research article
Guangyu Li
Chinese Academy of Agricultural Sciences Institute of Special Animal and Plant Sciences
Corresponding Author
License:
This work is licensed under a CC BY 4.0 License. Read Full License
Background
Self-injurious behavior (SIB) is a clinically challenging problem within both the general population and several clinical disorders. However, the precise molecular mechanism of SIB is still confused, and few animal models exist. Here, we systematic investigated the genesis and development of SIB based on behavioral and pathophysiology study in mink (Neovison vison) models.
Method
We used night-vision video to observe the mink behavior for four weeks,HE stain was performed to characteristic the pathology change of brain. We performed IHC assay to detect the protein level of Iba-1、p-CREB 、CBP and p300 in the brain tissues. Elisa assay used to examined the levels of NfL and NfH in serum and CSF of mink. qRT-PCR assay was mused to detected the expression of Bcl2, NOR1, FoxO4、c-FOS、CBP and p300 in brain tissues. Western blot was used to detect the protein levels of p-CREB、CBP and p300 in brain tissues. We also used Evans Blue as a tracer to detect whether the blood brain barrier was impaired in the brain of mink.
Rusult
First we combine behavioral testing, histopathological and molecular biology experiments found that CBP was related with SIB. Mechanism analysis showed that the dysregulation of CBP in brain activated CREB signaling, resulting in nerve damage of brain and SIB symptoms in minks. Importantly, the CBP-CREB interaction inhibitor helped to relieve SIB and nerve damage in brain tissues.
Conclusion
Our results illustrate an induction of CBP and an activation of CREB, as a novel mechanism in the genesis of SIB. These finding indicate that CBP-CREB axis is critical for SIB and demonstrate the efficacy of the CBP-CREB interaction inhibitor in treating these behaviors.
Keywords
Self-injury behavior (SIB), mink, nerve damage, CBP, p-CREB
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This is a preprint. It has not completed peer review.
Research article
Guangyu Li
Chinese Academy of Agricultural Sciences Institute of Special Animal and Plant Sciences
Corresponding Author
Badges
Prescreen
This manuscript passed our Prescreen assessment
Complete author information
Appropriate declaration statements
Potential risks to human health
Prescreen
History
CURRENT STATUS: Posted
Version 1
Posted 17 Jul, 2020
No community comments so far
Metrics
Comments: 0
PDF Downloads: ...
HTML Views: ...
License:
This work is licensed under a CC BY 4.0 License. Read Full License
Background
Self-injurious behavior (SIB) is a clinically challenging problem within both the general population and several clinical disorders. However, the precise molecular mechanism of SIB is still confused, and few animal models exist. Here, we systematic investigated the genesis and development of SIB based on behavioral and pathophysiology study in mink (Neovison vison) models.
Method
We used night-vision video to observe the mink behavior for four weeks,HE stain was performed to characteristic the pathology change of brain. We performed IHC assay to detect the protein level of Iba-1、p-CREB 、CBP and p300 in the brain tissues. Elisa assay used to examined the levels of NfL and NfH in serum and CSF of mink. qRT-PCR assay was mused to detected the expression of Bcl2, NOR1, FoxO4、c-FOS、CBP and p300 in brain tissues. Western blot was used to detect the protein levels of p-CREB、CBP and p300 in brain tissues. We also used Evans Blue as a tracer to detect whether the blood brain barrier was impaired in the brain of mink.
Rusult
First we combine behavioral testing, histopathological and molecular biology experiments found that CBP was related with SIB. Mechanism analysis showed that the dysregulation of CBP in brain activated CREB signaling, resulting in nerve damage of brain and SIB symptoms in minks. Importantly, the CBP-CREB interaction inhibitor helped to relieve SIB and nerve damage in brain tissues.
Conclusion
Our results illustrate an induction of CBP and an activation of CREB, as a novel mechanism in the genesis of SIB. These finding indicate that CBP-CREB axis is critical for SIB and demonstrate the efficacy of the CBP-CREB interaction inhibitor in treating these behaviors.
Figure 1
Figure 2
Figure 3
Figure 4
Figure 5
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