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
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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