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  • Title: Aminoguanidine reverses cognitive deficits and activation of cAMP/CREB/BDNF pathway in mouse hippocampus after traumatic brain injury (TBI).
    Author: Wang W, Shen M, Sun K, Wang Y, Wang X, Jin X, Xu J, Ding L, Sun X.
    Journal: Brain Inj; 2018; 32(13-14):1858-1865. PubMed ID: 30346862.
    Abstract:
    PRIMARY OBJECTIVE: We aim to study the effects of chronic aminoguanidine (AG) administration on learning and memory impairment after TBI and explore the potential mechanism involved in this process. RESEARCH DESIGN: Male C57BL/6J mice were divided into 6 groups: Control, TBI + Veh, TBI+ AG (50, 100, 200 and 400 mg/kg, i.p.). METHODS AND PROCEDURES: Then, we measured cyclicadenosine 3', 5'-monophosphate (cAMP) content, phosphorylated form of cAMP-response element binding protein (p-CREB) level, iNOS, brain-derived neurotrophic factor (BDNF) and postsynaptic density-93/95 (PSD-93/95) expression in hippocampus. The learning and memory abilities were assessed using Morris water maze and step-down test. MAIN OUTCOMES AND RESULTS: The results demonstrate that TBI induced down-regulation of BDNF, loss of PSD-93/95, learning and memory deficits with down-regulation of cAMP content and p-CREB/CREB ratio. Administration of AG (200 and 400 mg/kg) reversed TBI induced down-regulation of BDNF and PSD-93/95, up-regulated the cAMP content and p-CREB/CREB ratio, which resulted in improvement of learning and memory ability. CONCLUSIONS: We suspect that AG (200 and 400 mg/kg) might reverse TBI-induced selective loss of postsynaptic proteins and learning and memory deficits with the activation of cAMP/CREB/BDNF signalling pathway.
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