Brain Imaging and Ultrastructural Studies of the Effect of Electroacu-puncture on Improving Learning and Memory Impairments in the Focal Cerebral Ischemia Rats

Cordycepin exerted significant neuroprotective effects and protected against cerebral ischemic damage. Learning and memory impairments after cerebral ischemia are common. Cordycepin has been proved to improve memory impairments induced by cerebral ischemia, but its underlying mechanism has not been revealed yet. The plasticity of synaptic structure and function is considered to be one of the neural mechanisms of learning and memory. Therefore, we investigated how cordycepin benefits dendritic morphology and synaptic transmission after cerebral ischemia and traced the related molecular mechanisms. The effects of cordycepin on the protection against ischemia were studied by using global cerebral ischemia (GCI) and oxygen-glucose deprivation (OGD) models. Behavioral long-term potentiation (LTP) and synaptic transmission were observed with electrophysiological recordings. The dendritic morphology and histological assessment were assessed by Golgi staining and hematoxylin-eosin (HE) staining, respectively. Adenosine A1 receptors (A1R) and adenosine A2A receptors (A2AR) were evaluated with western blotting. The results showed that cordycepin reduced the GCI-induced dendritic morphology scathing and behavioral LTP impairment in the hippocampal CA1 area, improved the learning and memory abilities, and up-regulated the level of A1R but not A2AR. In the in vitro experiments, cordycepin pre-perfusion could alleviate the hippocampal slices injury and synaptic transmission cripple induced by OGD, accompanied by increased adenosine content. In addition, the protective effect of cordycepin on OGD-induced synaptic transmission damage was eliminated by using an A1R antagonist instead of A2AR. These findings revealed that cordycepin alleviated synaptic dysfunction and dendritic injury in ischemic models by modulating A1R, which provides new insights into the pharmacological mechanisms of cordycepin for ameliorating cognitive impairment induced by cerebral ischemia.

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Preconditioning with sevoflurane ameliorates spatial learning and memory deficit after focal cerebral ischemia–reperfusion in rats

International Journal of Developmental Neuroscience ◽

10.1016/j.ijdevneu.2013.04.004 ◽

2013 ◽

Vol 31 (5) ◽

pp. 328-333 ◽

Cited By ~ 13

Author(s):

Xianwen Hu ◽

Ye Zhang ◽

Weiyan Li ◽

Jian Liu ◽

Yun Li

Keyword(s):

Cerebral Ischemia ◽

Learning And Memory ◽

Spatial Learning ◽

Focal Cerebral Ischemia ◽

Ischemia Reperfusion ◽

Memory Deficit ◽

Spatial Learning And Memory ◽

Cerebral Ischemia Reperfusion ◽

Learning And Memory Deficit

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Chronic treatment of 4-phenylbutyric acid ameliorates cognitive impairment after focal cerebral ischemia/ reperfusion injury in rats

Indian Journal of Physiology and Pharmacology ◽

10.25259/ijpp_172_2020 ◽

2021 ◽

Vol 64 ◽

pp. 188-194

Author(s):

Kakarla Ramakrishna ◽

Krishnamoorthy Srinivasan ◽

Shyam Sunder Sharma

Keyword(s):

Cognitive Impairment ◽

Cerebral Ischemia ◽

Learning And Memory ◽

Focal Cerebral Ischemia ◽

Ischemia Reperfusion ◽

Motor Deficits ◽

Avoidance Task ◽

Neurological Score ◽

Y Maze ◽

Phenylbutyric Acid

Objectives: Stroke, apart from causing physical disabilities, it also often leads to cognitive impairment in patients. At present, there is no effective drug available for the treatment of post-stroke cognitive impairment. The present study was undertaken to evaluate the ameliorative effect of 4-Phenylbutyric acid (PBA) against cognitive and memory deficits due to focal cerebral ischemia/reperfusion (I/R) in rats. Materials and Methods: Focal cerebral I/R injury was achieved by the middle cerebral artery occlusion (MCAO) method. PBA (100 and 300 mg/kg, i.p.) was administered once daily for 2 weeks. The neurological score was counted to evaluate the severity of neurological motor deficits. The cognitive functions, including learning and memory, were assessed using various paradigms such as Y-maze, passive avoidance task and Morris water maze. Results: The chronic treatment of PBA (100 and 300 mg/kg, i.p.) dose-dependently improved the neurological motor deficits as shown by significant decrease in neurological score in MCAO-treated rats. Besides, PBA (100 and 300 mg/kg, i.p.) treatment markedly improved working memory as shown by significant increase in the relative percentage alternations compared to untreated control MCAO rats in Y-maze. PBA also significantly decreased the transfer latency in the acquisition trial and increased in probe trial in passive avoidance task suggesting an improvement in learning and memory in MCAO rats. There was also a significant improvement in spatial learning and memory, as evidenced by the reduced escape latency in acquisition trial and the increased number of entries into the platform zone, time spent in the platform quadrant and track plot in probe trial PBA-treated MCAO rats during Morris water maze task. Conclusion: This study, thus, demonstrates the potential of PBA in ameliorating cognitive dysfunctions in focal cerebral ischemia. Since PBA is already available for the treatment of urea cycle disorders, it may also be investigated for repurposing its use in the treatment of post-stroke cognitive impairment.

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