Degeneration of CA1 neurons in hippocampus after ischemia in Mongolian gerbils: cyclic AMP-systems.

Bilateral ischemia induced by occlusion of the carotid arteries for 5 min causes a selective degeneration of CA 1 neurons of the hippocampus of Mongolian gerbils. The degeneration process is complete in 14 days as assessed by light microscopy. After one week, basal values for radioactive cyclic AMP in [3H]adenine-labeled tissue from the CA 1 region of hippocampus are greatly reduced as are the absolute magnitude of accumulations of cyclic AMP elicited by norepinephrine, 2-chloroadenosine and histamine. At 2 and 4 weeks, basal values for radioactive cyclic AMP have nearly attained control values and the response to 2-chloroadenosine is fully restored. The response of cyclic AMP-generating systems to norepinephrine is now significantly greater than in control, while the response to histamine remains reduced in magnitude. The ischemia has no effect on basal values for radioactive cyclic AMP or on responses in [3H]adenine-labeled slices from cerebral cortex. Histamine levels after ischemia are significantly increased above control in the CA 1 region. Basal and histamine-sensitive adenylate cyclase activity in the membrane preparations are slightly decreased during the first week after ischemia, followed by a recovery. There is an inverse correlation between histamine levels and adenylate cyclase activity in individual animals 4 days after ischemia.