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The cellular mechanisms by which disruption of astrocytic IGF-1/IGF1R signaling impairs NVC responses likely include dysregulation of metabotropic glutamate receptors, NMDA receptors, and glutamate transporters [14, 17], upregulation of soluble epoxy hydrolase (which eliminates vasodilator EETs produced during astrocyte activation), and altered expression of cytochrome P450 enzymes [14]
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