Table 1.
Epigenetic-based treatments associated with manipulation of neurogenesis in mammals
Experimental system | Organism | Epigenetic drug | Functional effect | Ref. |
---|---|---|---|---|
Neural progenitor cells | Rat | VPA | Promotion of neuronal fate, inhibition of glial fate | [46] |
Adrenomedullary sympathoadrenal progenitors | Bovine | VPA | Promotion of catecholaminergic neuronal differentiation | [58] |
Brain neuroblastoma | Mouse | TSA | Induction of neurite extension | [201] |
Cerebella granule neurons | Rat | TSA | Promotion of neuronal outgrowth | [202] |
Adrenal medulla progenitors | Rat | TSA, VPA | Induction of neurite outgrowth | [60] |
Neural progenitor cells | Mouse | JQ-1 | Promotion of neurogenesis, inhibition of gliogenesis | [63] |
Neural progenitor cells | Mouse | SAHA, TSA | Reduction in neurogenesis in the ganglionic eminences, increase in neurogenesis in the cortex | [203] |
Primary glial cultures and glioblastoma cells | Human | VPA | Alteration of glial cell morphology | [204] |
Neural stem cells | Rat | 5-AZA | Reduction of migrated neurons and differentiation | [205] |
Representative examples of studies are included. 5-AZA 5-aza-cytidine, SAHA suberoylanilide hydroxamic acid, TSA trichostatin A, VPA valproic acid