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Related Concept Videos

Ischemic Stroke ll: Pathophysiology01:15

Ischemic Stroke ll: Pathophysiology

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An ischemic stroke occurs when a cerebral blood vessel becomes obstructed, most often by a thrombus or embolus, interrupting the delivery of oxygen and glucose to brain tissue. Because neurons rely on continuous aerobic metabolism, energy failure begins within minutes of reduced perfusion. The region receiving the least blood flow becomes the infarct core, an area of irreversible cellular death. Surrounding this core lies the penumbra, a zone of hypoperfused but still viable tissue that is...
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Ischemic stroke is an acute cerebrovascular condition in which blood flow to a brain region is suddenly interrupted, leading to tissue infarction. Neurons depend on continuous oxygen and glucose supply, so even brief reductions in perfusion cause energy failure, ionic imbalance, and irreversible injury. Ischemic strokes are classified into thrombotic and embolic types based on their underlying mechanisms.Thrombotic MechanismsThrombotic stroke develops when a clot forms within a cerebral artery.
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Early Ischemia and Ionic ImbalanceWithin minutes of spinal cord injury, a secondary cascade begins, progressing over hours to weeks. Vascular damage reduces blood flow, causing ischemia and mitochondrial dysfunction. ATP depletion leads to ion pump failure, membrane depolarization, sodium influx, potassium efflux, and water accumulation, resulting in cellular swelling. Increased intracellular calcium further disrupts mitochondria and accelerates cellular injury.Excitotoxicity and Neuronal...
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A hemorrhagic stroke develops when a cerebral blood vessel ruptures, allowing blood to escape into the surrounding brain tissue, as in intracerebral hemorrhage (ICH), or into the subarachnoid space, as in subarachnoid hemorrhage (SAH). Because the skull is a rigid compartment, the sudden presence of extravascular blood rapidly increases intracranial pressure and compresses adjacent neural structures, leading to immediate tissue injury and impaired cerebral perfusion.Mass Effect and Primary...
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A Cell Culture Model for Studying the Role of Neuron-Glia Interactions in Ischemia
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Synaptic and extrasynaptic glutamate signaling in ischemic stroke.

Naijian Chao, Sheng-Tian Li1

  • 1Bio-X Institutes, Shanghai Jiao Tong University, Dongchuan Road 800, Shanghai, 200240, P.R. China. lstian@sjtu.edu.cn.

Current Medicinal Chemistry
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Summary

Ischemic stroke, a major cause of death, involves glutamate signaling in the central nervous system (CNS). This review explores glutamate

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Area of Science:

  • Neuroscience
  • Neurology
  • Pathophysiology

Background:

  • Stroke is a primary cause of mortality and disability, with ischemic stroke being the most common type.
  • The central nervous system (CNS) is highly susceptible to ischemic conditions due to high energy demands of synaptic transmission.
  • Excessive glutamate release during ischemia triggers detrimental signaling pathways, accelerating neuronal death and brain injury.

Purpose of the Study:

  • To provide a comprehensive overview of synaptic and extrasynaptic glutamate signaling in the context of ischemic stroke.
  • To elucidate the mechanisms by which glutamate contributes to neuronal damage and cerebral injury during stroke.
  • To offer insights into potential therapeutic strategies targeting glutamate signaling pathways.

Main Methods:

  • This is a review article, synthesizing existing research on glutamate signaling in ischemic stroke.
  • Literature search and analysis of recent discoveries in neuroscience and neurology related to glutamate.
  • Focus on understanding the dual role of glutamate at synaptic and extrasynaptic sites.

Main Results:

  • Elaborate synaptic transmission in the CNS consumes significant energy, compromising neuronal survival under ischemia.
  • Glutamate, when excessively released, initiates destructive signaling cascades at both synaptic and extrasynaptic locations.
  • These cascades are key drivers of neuronal apoptosis and the exacerbation of brain damage post-ischemic stroke.

Conclusions:

  • Understanding the intricate glutamate signaling network is crucial for developing effective ischemic stroke therapies.
  • Targeting specific aspects of glutamate signaling may offer novel therapeutic avenues to mitigate neuronal loss and functional deficits.
  • Further research into synaptic and extrasynaptic glutamate dynamics holds promise for improving patient outcomes.