Short-term lithium treatment protects the brain against ischemia–reperfusion injury by enhancing the neuroplasticity of cortical neurons
| Autor: | Sheng-Yang Huang, Tian Shung Wu, Che Chao Chang, Tung-Yi Huang, E-Jian Lee, Shih-Huang Tai, Liang-Chun Chao |
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| Rok vydání: | 2021 |
| Předmět: |
Lithium (medication)
Ischemia Pharmacology Neuroprotection Brain ischemia Evoked Potentials Somatosensory Cortex (anatomy) Neuroplasticity medicine Animals Cells Cultured Ischemic Stroke Cerebral Cortex Neuronal Plasticity business.industry Pyramidal Cells Infarction Middle Cerebral Artery General Medicine medicine.disease Rats Disease Models Animal Neuroprotective Agents medicine.anatomical_structure Neurology Somatosensory evoked potential Reperfusion Injury Lithium Compounds Neurology (clinical) business Reperfusion injury medicine.drug |
| Zdroj: | Neurological Research. 44:128-138 |
| ISSN: | 1743-1328 0161-6412 |
| DOI: | 10.1080/01616412.2021.1965427 |
| Popis: | Objectives Lithium exerts a broad neuroprotective effect on the brain. This study examined whether lithium exerts therapeutic effects on stroke by restoring neural connections at the ischemic core of cortices post brain insult. Methods We treated rats with lithium or vehicle (saline) every 24 h for the first 72 h, starting at the beginning of reperfusion after inducing middle cerebral artery occlusion (MCAO) in rats. Somatosensory evoked potential (SSEP) recording and behavioral testing were employed to evaluate the beneficial effects of lithium treatment. To examine the effects of lithium-induced neuroplasticity, we evaluated the dendritic morphology in cortex pyramidal cells and the primary neuronal cell culture that underwent brain insults and oxygen and glucose deprivation (OGD), respectively. Results The results demonstrated that rats subjected to MCAO had prolonged N1 latency and a decreased N1/P1 amplitude at the ipsilateral cortex. Four doses of lithium reduced the brain infarction volume and enhanced the SSEP amplitude. The results of neurobehavioral tests demonstrated that lithium treatment improved sensory function, as demonstrated by improved 28-point clinical scale scores. In vitro study results showed that lithium treatment increased the dendritic lengths and branches of cultured neurons and reversed the suppressive effects of OGD. The in vivo study results indicated that lithium treatment increased cortical spine density in various layers and resulted in the development of the dendritic structure in the contralateral hemisphere. Conclusion Our study confirmed that neuroplasticity in cortical neurons is crucial for lithium-induced brain function 50 recovery after brain ischemia. |
| Databáze: | OpenAIRE |
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