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Journal of Neuroscience, Vol 13, 3964-3979, Copyright © 1993 by Society for Neuroscience
Vulnerability of mossy fiber targets in the rat hippocampus to forebrain ischemia
M Hsu and G Buzsaki
Center for Molecular and Behavioral Neuroscience, Rutgers 07102.
Much of the work on forebrain ischemia in the hippocampus has focused on
the phenomenon of delayed neuronal death in CA1. It is established that
dentate granule cells and CA3 pyramidal cells are resistant to ischemia.
However, much less is known about interneuronal involvement in CA3 or
ischemic injury in the dentate hilus other than the fact that somatostatin
neurons in the latter lose their immunoreactivity. We combined two
sensitive methods--heat-shock protein (HSP72) immunocytochemistry and a
newly developed Gallyas silver stain for demonstrating impaired
cytoskeletal elements--to investigate the extent of ischemic damage to CA3
and the dentate hilus using the four-vessel- occlusion model for inducing
forebrain ischemia. HSP72-like immunoreactivity was induced in neuronal
populations previously shown to be vulnerable to ischemia. In addition, a
distinct subset of interneurons in CA3 was also extremely sensitive to
ischemia, even more so than the CA1 pyramidal cells. These neurons are
located in the stratum lucidum of CA3 and possess a very high density of
dendritic spines. In silver preparations, they were among the first to be
impregnated as "dark" neurons, before CA1 pyramidal cells; microglial
reaction was also initiated first in the stratum lucidum of CA3. Whereas
CA1 damage was most prominent in the septal half of the hippocampus, hilar
and CA3 interneuronal damage had a more extensive dorsoventral
distribution. Our results also show a far greater extent of damage in hilar
neurons than previously reported. At least four hilar cell types were
consistently compromised: mossy cells, spiny fusiform cells, sparsely spiny
fusiform cells, and long-spined multipolar cells. A common denominator of
the injured neurons in CA3 and the hilus was the presence of spines on
their dendrites, which in large part accounted for the far greater number
of mossy fiber terminals they receive than their non-spiny neighbors. We
suggest that the differential vulnerability of neuronal subtypes in these
two regions may be attributed to their extremely dense innervation by the
mossy fibers and/or the presence of non-NMDA receptor subtypes that are
highly permeable to calcium. In addition, early impairment of these spiny
CA3 cells and hilar neurons after ischemia may be causal to delayed
neuronal death in the CA1 pyramidal cells.
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