Rat optic nerve: disruption of gliogenesis with 5-azacytidine during early postnatal development.
The normal sequence of gliogenesis in the rat optic nerve was disrupted by neonatal treatment with the mitotic inhibitor 5-azacytidine (5-AZ). This protocol caused a marked reduction in the number of glial cells, especially oligodendrocytes, seen in 11- and 14-day-old animals. Myelin formation was also greatly reduced in animals of this age compared to controls, but optic nerve axons appeared to be well preserved. Electrophysiological studies demonstrated similar excitability properties and activity-evoked [K+] changes in normal and 5-AZ-treated nerves prior to 5 days of age. However, in older nerves there were striking changes in the compound action potential and activity-dependent K+ accumulation in 5-AZ-treated nerves compared to controls. This simple model of disrupted central nervous system gliogenesis should prove useful in analyzing a variety of questions regarding neuroglial interactions including the role of glial cells in ionic homeostasis of brain extracellular space.
B R
BR
Ransom
C L
CL
Yamate
J A
JA
Black
S G
SG
Waxman
D000818:Animals; D000831:Animals, Newborn / Q000254:growth & development*; D001374:Azacitidine / Q000494:pharmacology*; D004594:Electrophysiology; D005074:Evoked Potentials, Visual; D009186:Myelin Sheath / Q000503:physiopathology; D009457:Neuroglia / Q000187:drug effects* / Q000502:physiology; D009900:Optic Nerve / Q000254:growth & development / Q000503:physiopathology* / Q000648:ultrastructure; D051381:Rats; D011919:Rats, Inbred Strains
D001374:Azacitidine