ArticleIranian Red Crescent medical journal2015
Decreased Activity in Neuropathic Pain Form and Gene Expression of Cyclin-Dependent Kinase5 and Glycogen Synthase Kinase-3 Beta in Soleus Muscle of Wistar Male Rats.
Article in Iranian Red Crescent medical journal, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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2 citing papers in PubMed, 4 citations in OpenAlex.
- Combined Exercise and Ursolic Acid Improve Hippocampal Neuronal Markers and Exploratory-Locomotor Behavior in Aged Diabetic Rats.Journal of aging research · 2025Article
- Nutmeg oil alleviates chronic inflammatory pain through inhibition of COX-2 expression and substance P release in vivo.Food & nutrition research · 2016Article
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3 authors at 1 institution in 1 country.
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Abstract
backgroundThe relationship between decreased activity/neuropathic pain and gene expression alterations in soleus muscle has remained elusive.
objectivesIn this experimental study, we investigated the effects of decreased activity in neuropathic pain form on Cyclin-Dependent Kinase 5 (CDK5) and Glycogen Synthase Kinase-3 β (GSK-3β) gene expression in soleus muscle of rats. MATERIALS AND
methodsTwelve male Wistar rats were randomly divided into three groups: (1) tight ligation of the L5 spinal nerve (SNL: n = 4); (2) sham surgery (Sham: n = 4), and (3) control (C: n = 4). The threshold to produce a withdrawal response to a mechanical and thermal stimulus was measured using von Frey filaments and radiation heat apparatus, respectively. Following 4 weeks after surgery, the left soleus muscle was removed and mRNA levels were determined by real-time Polymerase Chain Reaction (PCR).
resultsCompared to control animals, L5 ligated animals developed mechanical and heat hypersensitivity during total period of study. Soleus muscle weight as well as CDK5 mRNA levels (less than ~ 0.4 fold) was decreased and GSK-3β mRNA levels (up to ~ 7 folds) increased in L5 ligated animals.
conclusionsThese results showed enhanced muscle atrophy processes following peripheral nerve damage and might provide a useful approach to study underlying muscle mechanisms associated with clinical neuropathic pain syndromes.
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