TRANSIENT FOREBRAIN ISCHEMIA-INDUCED NEURONAL DEGENERATION IN FASCIA-DENTATA TRANSPLANTS

Citation
N. Tonder et al., TRANSIENT FOREBRAIN ISCHEMIA-INDUCED NEURONAL DEGENERATION IN FASCIA-DENTATA TRANSPLANTS, Restorative neurology and neuroscience, 6(3), 1994, pp. 239-249
Citations number
54
Categorie Soggetti
Neurosciences
ISSN journal
09226028
Volume
6
Issue
3
Year of publication
1994
Pages
239 - 249
Database
ISI
SICI code
0922-6028(1994)6:3<239:TFINDI>2.0.ZU;2-E
Abstract
Fascia dentata tissue blocks from newborn rats were grafted into one-w eek-old, ibotenic acid-induced lesions of the fascia dentata, or the n ormal fascia dentata of adult rats. After at least 2 months survival t he recipient rats were subjected to 10 min of forebrain ischemia (4-ve ssel occlusion), and examined 2 or 4 days later for neuronal degenerat ion in the host hippocampi and the transplants, by silver staining and immunohistochemistry. Transplants survived well in both normal and le sioned host brains, with easily recognizable subfields and layers and presence of normal types of principal and non-principal neurons. As ex pected, argyrophilic, degenerating neurons were present in the pyramid al cell layer of CA1 and CA3c of the non-grafted contralateral host hi ppocampus and in the contralateral dentate hilus (CA4). In the hilus t he degeneration corresponded to the loss of somatostatin-immunoreactiv e neurons, while parvalbumin-immunoreactive neurons were spared. In th e dentate transplants degenerating neurons were observed in the granul e cell layer, the hilus and the adjacent CA3 pyramidal cell layer. The re was no obvious loss of either somatostatin- or parvalbumin-immunore active neurons. The degeneration varied considerably between transplan ts, from a few to large groups of silver stained neurons, but this dif ference did not display any obvious relation to grafting into normal o r lesioned hosts, the exact location of the grafts or the general orga nization and distribution of intrinsic or extrinsic host afferents in the grafts. The results demonstrate that both ischemia-susceptible and -resistant types of neurons grafted to normal and lesioned adult rat brains are susceptible to transient forebrain ischemia after transplan tation. In spite of an extensive reorganization of transplant nerve co nnections, the physiologicalbiochemical mechanisms necessary for the i nduction of ischemic cell death were accordingly present in the transp lants.