title: Expression of zinc-positive cells and terminals in fetal neocortical homografts to adult rat depends on lesion type and rearing conditions.
abstract: Zinc-positive neurons and terminals, known to be associated with the glutamatergic projections in the brain, can be demonstrated by the histochemical Timm method and later modifications thereof. The adult rat neocortex contain a uniform lamination of zinc-positive cells with specific projections to, e.g., the striatum. We have previously reported that fetal neocortical grafts implanted in the adult rat neocortex combined with rearing in an enriched environment can improve behavioral functions and reduce the secondary atrophy of thalamus after cortex infarction in adult rats. In order to examine whether the expression of zinc positivity is ontogenetically inherent to neocortical neurons we grafted fetal neocortical tissue to aspiration or ischemic lesions of the frontoparietal neocortex of adult rats, followed by histochemical visualization of the vesicular zinc pool by selenite or sulfide. One further aim of the study was to elucidate to what extent the distribution of zinc-containing neurons and terminals in the grafts depended on rearing under different environmental conditions. The foremost finding of the present study was that the overall density of zinc-containing terminals in fetal cortical transplants placed in brain infarcts of adult spontaneously hypertensive rats is higher when the rats are reared in an enriched environment. Moreover, the presence and expression of zinc-positive neurons and terminals do not seem to be ontogenetically inherent to the cortical neurons as the fetal neocortical grafts placed in aspiration lesions contained no zinc-selenide-positive neurons and few or no zinc-selenide-positive terminals. The presence or expression of zinc-positive cells may thus be induced by ingrowth of fibers and terminals from the host brain as transplants placed in the ischemic lesions expressed both zinc-positive neurons and terminals.
authors.affiliation: Experimental Neurology, Lund University Hospital, Lund, Sweden.
authors.forename: J
authors.initials: J
authors.lastname: Zeng
authors.forename: B
authors.initials: B
authors.lastname: Mattsson
authors.forename: M K
authors.initials: MK
authors.lastname: Schulz
authors.forename: B B
authors.initials: BB
authors.lastname: Johansson
authors.forename: J C
authors.initials: JC
authors.lastname: Sørensen
mesh_terms: D000818:Animals; D001522:Behavior, Animal; D002545:Brain Ischemia / Q000378:metabolism / Q000601:surgery*; D016380:Brain Tissue Transplantation; D002452:Cell Count; D002541:Cerebral Decortication; D002799:Cholinergic Fibers / Q000378:metabolism; D004777:Environment; D016332:Fetal Tissue Transplantation; D006085:Graft Survival; D006973:Hypertension / Q000378:metabolism; D020244:Infarction, Middle Cerebral Artery; D008297:Male; D019579:Neocortex / Q000166:cytology / Q000378:metabolism* / Q000601:surgery / Q000637:transplantation*; D009474:Neurons / Q000166:cytology / Q000378:metabolism* / Q000637:transplantation; D017729:Presynaptic Terminals / Q000378:metabolism*; D051381:Rats; D011918:Rats, Inbred SHR; D011921:Rats, Inbred WKY; D018036:Selenium Compounds / Q000032:analysis / Q000378:metabolism; D018038:Sodium Selenite / Q000378:metabolism; D013440:Sulfides / Q000032:analysis / Q000378:metabolism; D015032:Zinc / Q000378:metabolism*; D017967:Zinc Compounds / Q000032:analysis / Q000378:metabolism
chemical_list: D018036:Selenium Compounds; D013440:Sulfides; D017967:Zinc Compounds; D018038:Sodium Selenite; D015032:Zinc; C031238:zinc sulfide; C044696:zinc selenide; C033479:sodium sulfide