N. Tonder et al., TRANSIENT FOREBRAIN ISCHEMIA-INDUCED NEURONAL DEGENERATION IN FASCIA-DENTATA TRANSPLANTS, Restorative neurology and neuroscience, 6(3), 1994, pp. 239-249
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.