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Description
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]
10.3390/antiox8090413 55 LassmannH
Prog Neuropsychopharmacol Biol Psychiatry 2009
doi: 10.1519/JSC.0000000000001971
