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In the glutamatergic synapses where ICAM-5 is expressed, N-methyl--aspartic acid (NMDA) receptor signaling removes the ICAM-5 block.This leads to shedding of the extracellular part of ICAM-5 (Tian et al., 2007).
ICAM-5 is expressed on the dendrites and soma of neurons of the telencephalon, with the highest level of expression in the glutamatergic neurons of the hippocampus and cerebral cortex.
As the spines mature, ICAM-5 migrates away from the postsynaptic density to the spine shafts.
During early development, ICAM-5 induces neurite sprouting, supposedly through homophilic binding (Tian et al., 2000b).
ICAM-5 further reduced the secretion of the proinflammatory cytokines tumor necrosis factor α (TNF-α) and interleukin 1β (IL-1β), but on the contrary induced the secretion of the anti-inflammatory IL-10 from lipopolysaccharide (LPS) stimulated microglia.
Thus, ICAM-5 might be involved in the regulation of microglia in both health and disease, playing an important neuroprotective role when the brain is under immune challenges and as a “don’t-eat-me” signal when it is solubilized from active synapses.