Molecular Communication of a Dying Neuron in Stroke

Abstract

When a main artery of the brain occludes, a cellular response involving multiple cell types follows. Cells directly affected by the lack of glucose and oxygen in the neuronal core die by necrosis. In the periphery surrounding the ischemic core (the so-called penumbra) neurons, astrocytes, microglia, oligodendrocytes, pericytes, and endothelial cells react to detrimental factors such as excitotoxicity, oxidative stress, and inflammation in different ways. The fate of the neurons in this area is multifactorial, and communication between all the players is important for survival. This review focuses on the latest research relating to synaptic loss and the release of apoptotic bodies and other extracellular vesicles for cellular communication in stroke. We also point out possible treatment options related to increasing neuronal survival and regeneration in the penumbra.

Ischemia-Triggered Glutamate Excitotoxicity From the Perspective of Glial Cells

“…Ischemia is a medical condition in which poor blood flow to the tissue causes oxygen and glucose deprivation (OGD), both leading to cell death (Puig et al, 2018). A fall in the number of neurons, followed by a decrease in the counts of glia is apparent especially in the brain parenchyma, due to its high demand for aerobic metabolism.…”

Decoding the transcriptional response to ischemic stroke in young and aged mouse brain

“…Pathophysiology of ischemic stroke is complex, and involves various mechanisms including disruption of bloodbrain barrier (BBB), excitotoxicity, inflammation, oxidative damage, ionic imbalances, apoptosis, angiogenesis and neuroprotection. The ultimate result of ischemic cascade is neuronal death along with an irreversible loss of neuronal function 6,7 . Two main approaches considered to treat acute ischemic stroke are reperfusion (restoration of blood flow) and neuroprotection (protection of neurons from ischemic injury) 8,9 .…”

Modes of Calcium Regulation in Ischemic Neuron

“…This arises as conflicting opinions as to whether NCX is neuroprotective or neuroimaging. Under these conditions-blocking NCX activity is neuroprotective [27]. In contrast, after milder episodes of cerebral ischemia, which normally results in neuronal recovery of delayed neuronal death, the NCX operates in calcium exit mode in an attempt to restore calcium homeostasis.…”