title: Progressive brain damage and alterations in dendritic arborization after collagenase-induced intracerebral hemorrhage in rats.
abstract: Intracerebral hemorrhage (ICH) was widely believed to be a monophasic event whereby cell death occurs from the initial space-occupying effects of the hematoma. However, we now know that secondary degenerative events contribute to delayed cell death, functional impairment and clinical deterioration. In three experiments, we further characterized the long-term maturation of injury in the collagenase model of striatal ICH in rat. First, we quantified the volume of tissue lost from 7 to 60 days showing that tissue loss more than doubled over this time. As the volume of tissue lost does not distinguish gray from white matter damage, gold chloride staining was used in a second experiment in ICH rats that survived 7 or 60 days. The mid-sagittal area of the corpus callosum significantly declined (22%) over this period, whereas the hippocampal and anterior commissures were not affected. A third experiment used the Golgi-Cox stain to examine dendritic arborization of peri-hematoma and contralateral medium spiny neurons of the striatum. We found an early and sustained increase in dendritic arborization in the non-lesioned hemisphere, whereas there was initial atrophy of peri-hematoma striatal neurons that eventually recovered to normal. These findings show that tissue loss, including white matter atrophy, continues over extended periods after ICH making it a potential target for cytoprotective agents. Finally, the dendritic alterations in both ipsi- and contralateral striatal neurons likely influence spontaneous recovery and are potential targets to further improve it.
authors.affiliation: Centre for Neuroscience, University of Alberta, Edmonton, AB, Canada.
authors.forename: Angela P
authors.initials: AP
authors.lastname: Nguyen
authors.forename: Hang D
authors.initials: HD
authors.lastname: Huynh
authors.forename: Suzanne B
authors.initials: SB
authors.lastname: Sjovold
authors.forename: Frederick
authors.initials: F
authors.lastname: Colbourne
mesh_terms: D000818:Animals; D001284:Atrophy / Q000209:etiology / Q000473:pathology / Q000503:physiopathology; D002536:Cerebral Arteries / Q000187:drug effects / Q000473:pathology / Q000503:physiopathology; D002543:Cerebral Hemorrhage / Q000139:chemically induced / Q000150:complications*; D017364:Collagenases; D004396:Coloring Agents; D003337:Corpus Callosum / Q000473:pathology / Q000503:physiopathology; D003342:Corpus Striatum / Q000473:pathology / Q000503:physiopathology; D003712:Dendrites / Q000473:pathology*; D004195:Disease Models, Animal; D018450:Disease Progression; D017612:Gold Compounds; D008297:Male; D009410:Nerve Degeneration / Q000209:etiology* / Q000473:pathology* / Q000503:physiopathology; D009413:Nerve Fibers, Myelinated / Q000473:pathology; D051381:Rats; D017207:Rats, Sprague-Dawley; D016622:Silver Staining; D013194:Staining and Labeling
chemical_list: D004396:Coloring Agents; D017612:Gold Compounds; C038016:gold chloride; D017364:Collagenases