Anxiolytic effect of CPEB1 knockdown on the amygdala of a mouse model of inflammatory pain
Autor: | Ming-gao Zhao, Hai-yan Liu, Jiao Yue, Shui-bing Liu, Yan-yan Guo, Xin-shang Wang, Li-ning Hu, Kai-yin Zheng |
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Rok vydání: | 2018 |
Předmět: |
Male
0301 basic medicine medicine.drug_class Cytoplasmic polyadenylation element Freund's Adjuvant Genetic Vectors Pain Anxiety Neurotransmission Inhibitory postsynaptic potential Synaptic Transmission Amygdala Anxiolytic 03 medical and health sciences 0302 clinical medicine Receptors GABA MRNA polyadenylation medicine Animals Receptors AMPA RNA Small Interfering Cells Cultured Inflammation Neurons mRNA Cleavage and Polyadenylation Factors Basolateral Nuclear Complex business.industry General Neuroscience Neural Inhibition Hindlimb Mice Inbred C57BL Disease Models Animal 030104 developmental biology medicine.anatomical_structure Gene Knockdown Techniques medicine.symptom business Disks Large Homolog 4 Protein Neuroscience 030217 neurology & neurosurgery Transcription Factors Basolateral amygdala |
Zdroj: | Brain Research Bulletin. 137:156-165 |
ISSN: | 0361-9230 |
Popis: | Anxiety disorders are a category of mental disorders characterized by feelings of anxiety, stress, and fear attached to various sources. However, their pathogenesis is complicated and has not been fully elucidated. The amygdala is a vital brain region that regulates anxiety and mental disorders. Cytoplasmic polyadenylation element binding protein 1 (CPEB1) mediates the extension of the mRNA polyadenylation tail and facilitates the translation of target RNA. CPEB1 is closely related to neuronal diseases, such as Fragile X Syndrome, learning and memory disorders, and chronic pain. In this study, the role of CPEB1 in anxiety development was determined in a pain-mediated anxiety mouse model. The anxiety model was established in mice by injecting with Complete Freund's Adjuvant (CFA) into the hindpaw. CFA injection then led to anxiety-like behaviors and increased the CPEB1 levels in the mouse basolateral amygdala (BLA). CPEB1 enhancement facilitated the translation of GluA1, GluN2A, GluN2B, PSD95, and GABA receptors, which disturbed the E/I balance in the BLA as shown by enhanced excitatory presynaptic release and reduced inhibitory presynaptic release. CPEB1 knockdown with AAV-CPEB1-shRNA alleviated the anxiety-like behaviors but not the pain-like behaviors by enhancing inhibitory transmission in the BLA of model mice. The data suggest that CPEB1 participates in anxiety development by regulating excitatory/inhibitory synaptic transmission in the BLA. |
Databáze: | OpenAIRE |
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