Lithium upregulates growth-associated protein-43 (GAP-43) and postsynaptic density-95 (PSD-95) in cultured neurons exposed to oxygen-glucose deprivation and improves electrophysiological outcomes in rats subjected to transient focal cerebral ischemia following a long-term recovery period
| Autor: | Shih-Huang, Tai, Sheng-Yang, Huang, Liang-Chun, Chao, Yu-Wen, Lin, Chien-Chih, Huang, Tian-Shung, Wu, Yan-Shen, Shan, Ai-Hua, Lee, E-Jian, Lee |
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| Rok vydání: | 2022 |
| Předmět: |
Male
Neurons Glycogen Synthase Kinase 3 beta N-Methylaspartate Brain-Derived Neurotrophic Factor Sodium Dodecyl Sulfate Infarction Middle Cerebral Artery General Medicine Lithium Receptors N-Methyl-D-Aspartate Brain Ischemia Rats Oxygen Rats Sprague-Dawley GAP-43 Protein Glucose Neuroprotective Agents Neurology Animals Neurology (clinical) Lithium Chloride Disks Large Homolog 4 Protein Edetic Acid |
| Zdroj: | Neurological Research. 44:870-878 |
| ISSN: | 1743-1328 0161-6412 |
| DOI: | 10.1080/01616412.2022.2056817 |
| Popis: | Lithium has numerous neuroplastic and neuroprotective effects in patients with stroke. Here, we evaluated whether delayed and short-term lithium treatment reduces brain infarction volume and improves electrophysiological and neurobehavioral outcomes following long-term recovery after cerebral ischemia and the possible contributions of lithium-mediated mechanisms of neuroplasticity.Male Sprague Dawley rats were subjected to right middle cerebral artery occlusion for 90 min, followed by 28 days of recovery. Lithium chloride (1 mEq/kg) or vehicle was administered via intraperitoneal infusion once per day at 24 h after reperfusion onset. Neurobehavioral outcomes and somatosensory evoked potentials (SSEPs) were examined before and 28 days after ischemia-reperfusion. Brain infarction was assessed using Nissl staining. Primary cortical neuron cultures were exposed to oxygen-glucose deprivation (OGD) and treated with 2 or 20 μM lithium for 24 or 48 h; subsequent brain-derived neurotrophic factor (BDNF), growth-associated protein-43 (GAP-43), postsynaptic density-95 (PSD-95), and synaptosomal-associated protein-25 (SNAP-25) levels were analyzed using western blotting.Compared to controls, lithium significantly reduced infarction volume in the ischemic brain and improved electrophysiological and neurobehavioral outcomes at 28 days post-insult. In cultured cortical neurons, BDNF, GAP-43, and PSD-95 expression were enhanced by 24- and 48-h treatment with lithium after OGD.Lithium upregulates BDNF, GAP-43, and PSD-95, which partly accounts for its improvement of neuroplasticity and provision of long-term neuroprotection in the ischemic brain. |
| Databáze: | OpenAIRE |
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