Proliferation of Leptomeningeal Cells in Delayed Neuronal Death in Gerbils

Glial and vascular cell proliferation is known to be induced in several neurological disorders of the central nervous system. However, whether leptomeningeal cells proliferate in response to neuronal disorders including brain infarction or hemorrhage, remains unknown. We assessed 3H-thymidine incorporation into proliferating leptomeningeal cells in delayed neuronal death following a transient forebrain ischemia for 5 min in gerbils; the CA1 hippocampal neurons died 2-6 days after the ischemia. The number of 3H-labeled leptomeningeal cells started to increase 2 days after ischemia and reached 5 times that of the sham-operated animals 6 days after ischemia. The proliferative response was suppressed to the baseline level at 8 days after ischemia. The total number of leptomeningeal cells (3H-labeled and unlabeled cells) also started to increase 2 days after ischemia and reached 1.4 times at 4-8 days after that. These observations indicated that leptomeningeal cells begin to proliferate in response to ischemia-induced neuronal death in the central nervous system.