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Eighty minutes of Glycine or GABA\u2010A receptor activation produced a significant fall in the compound action potential recorded from isolated post\u2010natal day 10 rat optic nerve. This effect was largely reversed upon washout. Nicotinic acetylcholine receptor (nAChR) or adrenoreceptor activation with noradrenalin resulted in an \u223c35% block of the action potential that did not reverse during a 30\u2010min washout period. While the effect of nAChR activation was blocked by a nAChR antagonist, the effect of noradrenalin was not ablated by \u03b1\u2010 or \u03b2\u2010adrenoreceptor blockers applied alone or in combination. In the absence of noradrenalin, co\u2010perfusion with \u03b1\u2010 and \u03b2\u2010adrenoreceptor blockers resulted in nonreversible nerve failure indicating that tonic adrenoreceptor activation is required for nerve viability, while overactivation of these receptors is also damaging. Nerves exposed to nAChR + adrenoreceptor activation showed no axon pathology but had extensive glial injury revealed by ultrastructural analysis. Oligodendroglia exhibited regions of membrane vacuolization while profound changes were evident in astrocytes and included the presence of swollen and expanded mitochondria, vacuolization, cell processes disintegration, and membrane breakdown. Blinded assessment revealed higher levels of astrocyte injury than oligodendroglial injury. The findings show that overactivation of neurotransmitter receptors other than those for glutamate can produce extensive injury to developing white matter, a phenomenon that may be clinically significant. \u00a9 2009 Wiley\u2010Liss, Inc.<\/jats:p>","DOI":"10.1002\/glia.20839","type":"journal-article","created":{"date-parts":[[2009,1,23]],"date-time":"2009-01-23T19:12:28Z","timestamp":1232737948000},"page":"1168-1177","source":"Crossref","is-referenced-by-count":19,"title":["Conduction block and glial injury induced in developing central white matter by glycine, GABA, noradrenalin, or nicotine, studied in isolated neonatal rat optic 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