K. Yamashita et al., Involvement of glial endothelin/nitric oxide in delayed neuronal death of rat hippocampus after transient forebrain ischemia, CELL MOL N, 20(5), 2000, pp. 541-551
1. We examined time- and cell-type-dependent changes in endothelin (ET)-1-l
ike immunoreactivity, ET receptors binding and nitric oxide (NO) synthase (
NOS) activity in CA1 subfields of the hippocampus of stroke-prone spontaneo
usly hypertensive rats subjected to a 10-min bilateral carotid occlusion an
d reperfusion.
2. Microglia aggregated in accord with neuronal death and expressed a high
density of ETB receptors and an intense NOS activity in the damaged CA1 pyr
amidal cell layer, 7 days after the induced transient forebrain ischemia. T
he increased NOS activity and ETB receptor in microglia disappeared 28 days
after this transient ischemia.
3. In contrast to microglia, astrocytes presented a moderate level of ET-1-
like immunoreactivity, ETB receptors, and NOS activity in all areas of the
damaged CA1 subfields, 7 days after the ischemia. These events were further
enhanced 28 days after the ischemia.
4. In light of these findings, the possibility that the microglial and the
astrocytic ETB/ NO system largely contributes to development of the neurona
l death and to reconstitution of the damaged neuronal tissue, respectively,
in the hippocampus subjected to a transient forebrain ischemia would have
to be considered.