ArticleCNS neuroscience & therapeutics2025
CHOP-Mediated Disruption of Hippocampal Synaptic Plasticity and Neuronal Activity Contributes to Chronic Pain-Related Cognitive Deficits.
Article in CNS neuroscience & therapeutics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Targeting endoplasmic reticulum stress: a novel therapeutic strategy for neuropathic pain.Frontiers in pain research (Lausanne, Switzerland) · 2026Review
- Risk factors for postoperative cognitive dysfunction in geriatric trauma: a dual-pathway perspective.Frontiers in aging neuroscience · 2026Article
- ER stress-induced ITPR1/ANO1 signaling drives trigeminal neuropathic pain through calcium-dependent neuronal hyperexcitability.The journal of headache and pain · 2025Article
- miRNA-105 Attenuates Hypoxic-Ischemic Brain Damage in Neonatal Rats by Inhibiting Apoptosis and Necroptosis.Neurochemical research · 2025Article
- Chronic pain and cognitive dysfunction: clinical manifestations, underlying mechanisms, and emerging therapeutic strategies.Frontiers in neuroscience · 2025Review
- Folic Acid Ameliorates the Chronic Constriction Injury of Sciatic Nerve -Induced Memory Impairments in Rats.Iranian journal of pharmaceutical research : IJPRArticle
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Authors and funding
12 authors.
Funding
Abstract
objectivesEndoplasmic reticulum (ER) stress-induced protein homeostasis perturbation is a core pathological element in the pathogenesis of neurodegenerative diseases. This study aims to clarify the unique role played by C/EBP homologous protein (CHOP) as a biomarker of the unfolded protein response (UPR) in the etiology of chronic pain and related cognitive impairments following chronic constrictive nerve injury (CCI).
methodsThe memory capability following CCI was assessed utilizing the Morris water maze (MWM) and fear conditioning test (FCT). Activation of the UPR was quantified by assessing levels of CHOP and key ER stress sensors. The terminal deoxynucleotidyl transferase (TdT) dUTP nick-end labeling (TUNEL) assay and the levels of cleaved caspase-3 were utilized to assess apoptosis level. Synaptic plasticity was assessed via a modified Golgi-Cox staining method, and long-term potentiation (LTP) measurements were taken. Neuronal activity was determined by immunofluorescence and fiber photometry. Knockdown of CHOP and alleviation of ER stress were selectively induced by LV-Ddit3-shRNAs and the chemical chaperone 4-phenylbutyric acid (4-PBA), respectively.
resultsMice subjected to CCI displayed enduring pain and cognitive impairments evident on Days 21-28 post-surgery. Following CCI, changes in the dorsal CA1 (dCA1) manifested as ER dilation, upregulation of CHOP and upstream signaling molecules, reduced dendritic spine density, and PSD95 levels, and impaired LTP. Additionally, the co-localization of CaMKIIα/c-Fos and CaMKIIα
conclusionCCI-induced CHOP upregulation impairs dCA1 synaptic plasticity and neuronal activity, leading to chronic pain-related cognitive deficits.
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