Astrocyte‐induced synapse formation and ischemic stroke

Abstract

Astrocytes envelop synapses and blood vessels with their cellular projections, regulate their functions, and mediate varied effects in response to brain damage such as stroke (Gleichman & Carmichael, 2014). For example, astrocytes promote synaptic structure formation during the wrapping of dendritic spines and presynaptic terminals (Haber et al., 2006; Theodosis et al., 2008). In addition, changes in the structural relationships between astrocytic processes and dendritic spines regulate synaptic plasticity (Perez-Alvarez et al., 2014). Another function of astrocytes in neurotransmission is mediated through their glutamate transporters, ensuring glutamate clearance to maintain normal synaptic function. At excitatory synapses, astrocytes are localized more in the postsynaptic terminal region than in the presynaptic region, and glutamate transport functions to maintain low levels of glutamate around the postsynaptic side (Lehre & Rusakov, 2002). This difference in synaptic astrocyte localization also affects the amount of glutamate that escapes from the synaptic cleft, so that the degree of postsynaptic glutamate receptor activation is two to four times higher than that of the presynaptic (Lehre & Rusakov, 2002). Cholesterol-apolipoprotein E (ApoE) complexes secreted from astrocytes were the first-identified factor in synapse formation (Mauch et al., 2001). ApoE-cholesterol promotes synaptic function

ATPIF1 alleviates oxygen glucose deprivation/reoxygenation-induced astrocyte injury in vitro: A rat model of ischemic brain injury

“…Evidence of the relationship between ischemic brain injury and increased astrocyte injury has been found in previous research. 16 Astrocytes are the most abundant cell type in the central nervous system. 17 They communicate with neurons, oligodendrocytes and endothelial cells, and participate in maintaining normal brain function.…”

Crosstalk Between the Oxidative Stress and Glia Cells After Stroke: From Mechanism to Therapies

“…Glial cell-derived cholesterol serves as a raw material for synaptogenesis, promotes synaptogenesis and regulates myelin formation after stroke (149). Studies have reported that various molecules secreted by glial cells, such as TNF-a, thrombospondin, hevin have the ability to repair synaptic dysfunction after stroke (150). Beyond that, microglia and astrocytes secrete various nutrients and growth factors such as BDNF, nerve growth factor (NGF), and basic fibroblast growth factor (bFGF), which are useful for neural repair and plasticity (151,152).…”

Blockage of thrombospondin 4 secreted by spinal astrocytes may be a promising therapeutic target in the treatment of neuropathic pain

“…Astrocytes, one of the glial cells, modulate synapse formation and synaptic transmission in the CNS [44][45][46]. TSPs are a component of the intercellular signaling network mediated by astrocytes in the CNS [47,48], and astrocyte-derived TSPs are considered an essential synaptogenic signal in synaptogenesis [31,[48][49][50].…”