Cholinergic sprouting is blocked by repeated induction of electroconvulsive seizures, a manipulation that induces a persistent reactive state in astrocytes.
Previous studies have demonstrated that some of the molecular and morphological changes that are characteristic of reactive astrocytes are induced following seizures. This discovery provides the means to experimentally modify the time course and extent of reactive changes in astrocytes following injury and so explore how these reactive changes modulate other events in the injured nervous system. The present study evaluates whether superinduction of a reactive state in astrocytes alters one form of postlesion synaptic reorganization (the sprouting of cholinergic projections in the dentate gyrus after destruction of the entorhinal cortex). Cholinergic sprouting after entorhinal cortex lesions was evaluated in control mice and in mice that experienced electroconvulsive seizures (ECS) from the day of surgery until 12 days postlesion. Animals were prepared for acetylcholinesterase (AChE) histochemistry at 2, 4, 6, 8, 10, 12, 14, and 30+ days postlesion. Quantitative densitometric analyses revealed that the increase in AChE staining that is indicative of cholinergic sprouting was essentially eliminated in the animals that experienced daily ECS. These results indicate that the induction of electroconvulsive seizures during the postinjury period disrupts at least one form of postlesion synaptic reorganization that would otherwise occur. This disruption of synaptic reorganization may be a consequence of the induction of a persistent reactive state in astrocytes.
Steward
O
O
Department of Neuroscience, University of Virginia Health Sciences Center, Charlottesville 22908.
D000110:Acetylcholinesterase / Q000032:analysis / Q000096:biosynthesis*; D000704:Analysis of Variance; D000818:Animals; D001253:Astrocytes / Q000378:metabolism / Q000473:pathology*; D004597:Electroshock; D015870:Gene Expression; D005904:Glial Fibrillary Acidic Protein / Q000096:biosynthesis; D006624:Hippocampus / Q000378:metabolism / Q000473:pathology*; D017403:In Situ Hybridization; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D012333:RNA, Messenger / Q000032:analysis / Q000096:biosynthesis; D012640:Seizures / Q000378:metabolism / Q000473:pathology*; D013569:Synapses / Q000473:pathology; D013997:Time Factors
D005904:Glial Fibrillary Acidic Protein; D012333:RNA, Messenger; D000110:Acetylcholinesterase