Abstract
The cognitive impairment caused by cerebral ischemia/reperfusion is an unsolved problem in the field of international neural rehabilitation. Not only ameliorates the consciousness level of certain patients who suffered from ischemia-reperfusion injury and were comatose for a long time period after cerebral resuscitation treatment, but levodopa also improves the symptoms of neurological deficits in rats with global cerebral ischemia-reperfusion injury. However, Levodopa has not been widely used as a brain protection drug after cardiopulmonary resuscitation, because of its unclear repair mechanism. Levodopa was used to study the neuroplasticity in the hippocampus of global cerebral ischemia/reperfusion injury rat model, established by Pulsinelli's four-vessel occlusion method. Levodopa was injected intraperitoneally at 50 mg/kg/d for 7 consecutive days after 1st day of surgery. The modified neurological function score, Morris water maze, magnetic resonance imaging, Nissl and TH staining, electron microscopy and western blot were used in the present study. The results showed that levodopa improved the neurological function and learning and memory of rats after global cerebral ischemia/reperfusion injury, improved the integrity of white matter, and density of gray matter in the hippocampus, increased the number of synapses, reduced the delayed neuronal death, and increased the expression of synaptic plasticity-related proteins (BDNF, TrkB, PSD95, and Drebrin) in the hippocampus. In conclusion, levodopa can improve cognitive function after global cerebral ischemia/reperfusion injury by enhancing the synaptic plasticity in the hippocampus.
Highlights
Sudden cardiac arrest is caused by organic diseases of the heart or other reasons that stop the ejection function of the heart, and the arterial pulsation, which in turn interrupts the blood circulation (Myerburg and Goldberger, 2017)
The results showed that levodopa can up-regulate the optical density of Tyrosine Hydroxylase (TH)-stained sections in the rat hippocampus after GCI/R injury
Global cerebral ischemia/reperfusion causes delayed death of neurons in the hippocampus, unbalanced dopamine content, and decreased synaptic density, which eventually leads to learning and memory disorders
Summary
Sudden cardiac arrest is caused by organic diseases of the heart or other reasons that stop the ejection function of the heart, and the arterial pulsation, which in turn interrupts the blood circulation (Myerburg and Goldberger, 2017). This causes loss of consciousness and will subsequently result in serious hypoxia and ischemia of vital organs such as the heart, brain, and lungs. NMDAR blockers were extensively studied for the repair of cognitive impairment caused by neuropsychiatric diseases such as stroke and Alzheimer’s disease Due to their severe neurological side effects, most NMDAR blockers (such as MK801) ended in the failures related to the clinical studies (Zheng et al, 2017). The development of brain protection drugs after cardiopulmonary resuscitation has become a hot spot within the international neuroscience research field
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