During normal development of the central nervous system there is expression
of cyclins that regulate the progression of cells through various stages o
f mitosis. Cyclins have also been implicated in neuronal degeneration and a
poptosis in adult brain, especially cyclin DI as it is permissive for the t
ransition from growth phase to synthesis phase in mitotic cell division. Th
ere is controversy as to whether cyclin D1 expression increases in both in
vitro and in vivo models of cerebral ischemia. In this study we use immunoh
istochemistry and Western blot analysis to characterize cyclin D1 expressio
n in an in vivo rat global model of cerebral ischemia to address the hypoth
esis that cyclin DI alterations are involved in ischemic neuronal death. Al
though there was no change in cyclin D1 expression in either the vulnerable
CA1 or resistant CA3 regions of the hippocampus prior to neuronal cell dea
th (<3 days reperfusion), concomitant with the death of CAI neurons and the
loss of cyclin D1 in these cells, there was an increase in non-neuronal cy
clin D1 positive cells. Some of the non-neuronal cyclin D1 expressing cells
were identified to be activated microglia. In contrast to the cytoplasmic
expression of cyclin D1 in neurons, the cyclin D1 expression in the microgl
ia and other non-neuronal cells in CAI was both nuclear and cytosolic. This
study suggests that cyclin D1 does not play a role in the death of vulnera
ble CA1 neurons in global ischemia. (C) 2001 Elsevier Science B.V. All righ
ts reserved.