Abstract
Normal brain function is highly dependent on oxygen and nutrient supply and when the demand for oxygen exceeds its supply, hypoxia is induced. Acute episodes of hypoxia may cause a depression in synaptic activity in many brain regions, whilst prolonged exposure to hypoxia leads to neuronal cell loss and death. Acute inadequate oxygen supply may cause anaerobic metabolism and increased respiration in an attempt to increase oxygen intake whilst chronic hypoxia may give rise to angiogenesis and erythropoiesis in order to promote oxygen delivery to peripheral tissues. The effects of hypoxia on neuronal tissue are exacerbated by the release of many inflammatory agents from glia and neuronal cells. Cytokines, such as TNF-α, and IL-1β are known to be released during the early stages of hypoxia, causing either local or systemic inflammation, which can result in cell death. Another growing body of evidence suggests that inflammation can result in neuroprotection, such as preconditioning to cerebral ischemia, causing ischemic tolerance. In the following review we discuss the effects of acute and chronic hypoxia and the release of pro-inflammatory cytokines on synaptic transmission and plasticity in the central nervous system. Specifically we discuss the effects of the pro-inflammatory agent TNF-α during a hypoxic event.
Highlights
In the central nervous system, hypoxia occurs when there is an inadequate supply of oxygen to neuronal tissue
In critical cases of hypoxia-re-oxygenation the brain loses the ability to form new memories. This anterograde amnesia is decoupled from the hippocampus and its primarily caused by adenosine up-regulation of caspase 1 and IL-1β in the amygdala [34]
During an ischemic stroke and resulting hypoxia, inflammatory cytokines are released by microglia, neurons and astrocytes with glutamate largely released by neurons
Summary
In the central nervous system, hypoxia occurs when there is an inadequate supply of oxygen to neuronal tissue. An example of one such event with a hypoxic component is stroke, which is caused by a reduction in blood flow as a result of an obstruction or rupture of blood vessels within the brain and may cause both acute and chronic episodes of hypoxia. This leads to complex pathological changes taking place, which may lead to tissue necrosis through increased inflammation and oxygen deprivation [8]. In this review we will discuss how hypoxia and the release of pro-inflammatory cytokines can effect synaptic transmission and plasticity in the central nervous system (CNS)
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