Effects of altered gliogenesis on activity-dependent K+ accumulation in the developing rat optic nerve.
Gliogenesis in the rat optic nerve is disrupted by neonatal treatment with the mitotic inhibitor 5-azacytidine (5-AZ). The rate of myelination and number of glial cells are markedly reduced in treated animals. We analyzed the physiological consequences of these chemically induced morphological alterations in terms of activity-dependent K+ accumulation in brain extracellular space and characteristics of the compound action potential (CAP). Nerves from 5-AZ-treated animals older than 5 days of age showed significantly higher activity-dependent 'ceiling levels' of extracellular K+ concentration ( [K+]o) than controls. This result is consistent with the hypothesis that glial cells are involved in K+ homeostasis at a cellular level and play a role in helping to set the ceiling level of activity-dependent K+ accumulation. The CAPs of 5-AZ-treated nerves older than 5 days of age were larger and generally of simpler configuration than those observed in control animals, perhaps due, among other factors, to the retained uniformity of axonal conduction velocity caused by inhibition of myelination.
Yamate
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Ransom
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D000200:Action Potentials / Q000187:drug effects; D000367:Age Factors; D000818:Animals; D001374:Azacitidine / Q000494:pharmacology; D002452:Cell Count; D002455:Cell Division / Q000187:drug effects; D004558:Electric Stimulation; D009457:Neuroglia / Q000166:cytology* / Q000378:metabolism; D009900:Optic Nerve / Q000166:cytology* / Q000378:metabolism / Q000502:physiology; D011188:Potassium / Q000378:metabolism*; D051381:Rats; D011919:Rats, Inbred Strains; D011930:Reaction Time
D001374:Azacitidine; D011188:Potassium