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Translocator protein ligand, YL-IPA08, attenuates lipopolysaccharide-induced depression-like behavior by promoting neural regeneration

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Neural Regeneration Research 2018年第11期13卷 1937-1944页

作者： Xiao-Ying Zhang Li-Ming Zhang Wei-Dong Mi Yun-Feng Li Anesthesia and Operation Center Chinese PLA General Hospital Beijing China State Key Laboratory of Toxicology and Medical Countermeasures Beijing China

Translocator protein has received attention for its involvement in the pathogenesis of depression. This study assessed the effects of the new Translocator protein ligand, YL-IPA08, on alleviating inflammation-induced depression-like behavior in mice and investigated its mechanism of action. Mice were intracerebroventricularly injected with 1, 10, 100 or 1000 ng lipopolysaccharide. The tail-suspension test and the forced swimming test confirmed that 100 ng lipopolysaccharide induced depression-like behavior. A mouse model was then established by intraventricular injection of 100 ng lipopolysaccharide. On days 16-24 after model establishment, mice were intragastrically administered 3 mg/kg YL-IPA08 daily. Immunohistochemistry was used to determine BrdU and NeuN expression in the hippocampus. YL-IPA08 effectively reversed the depression-like behavior of lipopolysaccharide-treated mice, restored body mass, increased the number of BrdU-positive cells, and the number and proportion of BrdU and NeuN double-positive cells. These findings indicate that YL-IPA08 can attenuate lipopolysaccharide-induced depression-like behavior in mice by promoting the formation of hippocampal neurons.

关键词： nerve regeneration YL-IPA08 hippocampus dentate gyrus lipopolysaccharide neuroinflammation depression Translocator protein neural regeneration

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Application of modern neuroimaging technology in the diagnosis and study of Alzheimer’s disease

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Neural Regeneration Research 2021年第1期16卷 73-79页

作者： Hong-Mei Zeng Hua-Bo Han Qi-Fang Zhang Hua Bai Department of Neurology Third Affiliated Hospital of Guizhou Medical UniversityDuyunGuizhou ProvinceChina Department of Neurology Affiliated Hospital of Guizhou Medical UniversityGuiyangGuizhou ProvinceChina Department of Radiology Third Affiliated Hospital of Guizhou Medical UniversityDuyunGuizhou ProvinceChina Key Laboratory of Endemic and Ethnic Diseases of Ministry of Education and Key Laboratory of Medical Molecular BiologyGuizhou Medical UniversityGuiyangGuizhou ProvinceChina Medical Experiment Center Third Affiliated Hospital of Guizhou Medical UniversityDuyunGuizhou ProvinceChina

Neurological abnormalities identified via neuroimaging are common in patients with Alzheimer’s disease.However,it is not yet possible to easily detect these abnormalities using head computed tomography in the early stages of the disease.In this review,we evaluated the ways in which modern imaging techniques such as positron emission computed tomography,single photon emission tomography,magnetic resonance spectrum imaging,structural magnetic resonance imaging,magnetic resonance diffusion tensor imaging,magnetic resonance perfusion weighted imaging,magnetic resonance sensitive weighted imaging,and functional magnetic resonance imaging have revealed specific changes not only in brain structure,but also in brain function in Alzheimer’s disease patients.The reviewed literature indicated that decreased fluorodeoxyglucose metabolism in the temporal and parietal lobes of Alzheimer’s disease patients is frequently observed via positron emission computed tomography.Furthermore,patients with Alzheimer’s disease often show a decreased N-acetylaspartic acid/creatine ratio and an increased myoinositol/creatine ratio revealed via magnetic resonance imaging.Atrophy of the entorhinal cortex,hippocampus,and posterior cingulate gyrus can be detected early using structural magnetic resonance imaging.Magnetic resonance sensitive weighted imaging can show small bleeds and abnormal iron metabolism.Task-related functional magnetic resonance imaging can display brain function activity through cerebral blood oxygenation.Resting functional magnetic resonance imaging can display the functional connection between brain neural networks.These are helpful for the differential diagnosis and experimental study of Alzheimer’s disease,and are valuable for exploring the pathogenesis of Alzheimer’s disease.

关键词： Alzheimer’s disease behavior brain cognitive impairment fluorodeoxyglucose memory neurological function structural magnetic resonance imaging Translocator protein

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Elevated Neurosteroids in the Lateral Thalamus Relieve Neuropathic Pain in Rats with Spared Nerve Injury

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Neuroscience Bulletin 2016年第4期32卷 311-322页

作者： Meng Zhang Jia Liu Meng-Meng Zhou Honghai Wu Yanning Hou Yun-Feng Li Yuxin Yin Lemin Zheng Feng-Yu Liu Ming Yi You Wan Neuroscience Research Institute Peking UniversityBeiiing 100191 China Institute of Systems Biomedicine Peking UniversityBeijing 100191 China Department of Pharmacy Bethune International PeaceHospital Shijiazhuang Shijiazhuang 050082 China Department of New Drug Evaluation Beijing Institute ofPharmacology and Toxicology Beijing 100007 China Institute of Cardiovascular Sciences and Institute of SystemsBiomedicine and Key Laboratory of MolecularCardiovascular Sciences of the Ministry of Education PekingUniversity Beijing 100191 China Key Laboratory for Neuroscience Ministry of Education/National Health and Family Planning Commission School ofBasic Medical Sciences Peking University Beijing 100191China Department of Neurobiology School of Basic MedicalSciences Peking University Beijing 100191 China

Neurosteroids are synthesized in the nervous system from cholesterol or steroidal precursors imported from peripheral sources. These compounds are important allosteric modulators of γ-aminobutyric acid A receptors （GABAARs）, which play a vital role in pain modulation in the lateral thalamus, a main gate where somatosensory information enters the cerebral cortex. Using high-perfor mance liquid chromatography/tandem mass spectrometry, we found increased levels of neurosteroids （pregnenolone, progesterone, deoxycorticosterone, allopregnanolone, and tetrahydrodeoxycorticosterone） in the chronic stage of neuropathic pain （28 days after spared nerve injury） in rats.The expression of the Translocator protein TSPO, the upstream steroidogenesis rate-limiting enzyme, increased at the same time. In vivo stereotaxic microinjection of neurosteroids or the TSPO activator AC-5216 into the lateral thalamus （AP -3.0 mm, ML 4-3.0 mm, DV 6.0 mm） alleviated the mechanical allodynia in neuropathic pain, while the TSPO inhibitor PK 11195 exacerbated it. The analgesic effects of AC-5216 and neurosteroids were sig- nificantly attenuated by the GABAAR antagonist bicuculline. These results suggested that elevated neurosteroids in the lateral thalamus play a protective role in the chronic stage of neuropathic pain.

关键词： Neurosteroids Translocator protein Sparednerve injury Thalamus GABAA receptors

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