Involvement of canonical Wnt/β-catenin signaling in the extinction of auditory fear conditioning in male mice

Xu, Ning; Geng, Lian; Yan, Xianxia; Ai-jun, Niu; Yu, Hui; Su, Bo

doi:10.1016/j.bbr.2023.114378

Cited by 1 publication

(2 citation statements)

References 27 publications

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“…A strong functional interaction between CB1r and β-catenin has been suggested [30]. CB1r activation increases PI3K/AKT activity leading to GSK-3β phosphorylation, β-catenin stabilization, and its translocation into the nucleus; in the nucleus, β-catenin regulates transcription and gene expression to promote anti-stress responses [54,35,49,54]. Hence, URB597, acting through CB1r, modulates β-catenin that produces proresilient responses.…”

Section: The Effects Of Downregulating β-Catenin On Urb597 Modulation...mentioning

confidence: 99%

“…Wnt/β-catenin signaling was found to have a main role in various psychiatric conditions [33][34][35]. Specifically, β-catenin seems to be implicated in synaptic plasticity, particularly involving emotional learning and memory processes and appears to be involved in disorders associated with strong memory formation such as fear learning in PTSD [36] acting on fear retrieval through the medial PFC (mPFC) [37].…”

Section: Introductionmentioning

confidence: 99%

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Anandamide Hydrolysis Inhibition Modulates Stress Markers via Beta-Catenin in the PFC in A Rat Model Of PTSD

Akirav,

Portugalov,

Sbarski

et al. 2023

PNEURO

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Post-traumatic stress disorder (PTSD) involves dysregulation of stress modulators, particularly corticotrophin-releasing factor (CRF) and glucocorticoid receptor. Endocannabinoid )ECB( signaling usually serves to inhibit the stress response and has been suggested as a potential target for PTSD treatment. The Wnt/β-catenin pathway was found to play a significant role in anxiety and depression. We examined the expression of stress markers in the medial prefrontal cortex (mPFC) and basolateral amygdala (BLA) in a rat model for PTSD, and whether the stress-buffering effects of enhancing ECB signaling are mediated via β-catenin in the mPFC. Rats were exposed to the shock and reminders model for PTSD and injected with the fatty acid amide hydrolase (FAAH) inhibitor URB597 (0.4 mg/kg.). URB597 was found to normalize the dysregulation in stress markers in the mPFC and BLA as well as the anxiogenic phenotype. Importantly, downregulation by viral-mediated gene transfer of β-catenin in the mPFC blocked the stress-buffering effects of URB597 on CRF, a key modulator of the stress response, as well as on CB1r and β-catenin protein levels. We suggest a novel mechanism for the stress-buffering effects of FAAH inhibition on CRF that is dependent on β-catenin activation in the mPFC in a PTSD rat model.

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Section: The Effects Of Downregulating β-Catenin On Urb597 Modulation...mentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Anandamide Hydrolysis Inhibition Modulates Stress Markers via Beta-Catenin in the PFC in A Rat Model Of PTSD

Akirav,

Portugalov,

Sbarski

et al. 2023

PNEURO

View full text Add to dashboard Cite

show abstract

Involvement of canonical Wnt/β-catenin signaling in the extinction of auditory fear conditioning in male mice

Cited by 1 publication

References 27 publications

Anandamide Hydrolysis Inhibition Modulates Stress Markers via Beta-Catenin in the PFC in A Rat Model Of PTSD

Anandamide Hydrolysis Inhibition Modulates Stress Markers via Beta-Catenin in the PFC in A Rat Model Of PTSD

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