Effects of aging and chronic nimodipine on hippocampal binding of [3H]CGS 19755.

Previous studies have suggested that aging is associated with impaired behavioral performance and with decrements of N-methyl-D-aspartate (NMDA) receptors in the rat hippo-campus. Other studies have indicated that chronic treatment with nimodipine, a Ca2+ channel antagonist, prevents the age-related decline in performance by rats in behavioral tasks. Therefore, we tested whether nimodipine altered binding of [3H]CGS 19755 to hippocampal NMDA receptors in rats whose performance on a 14-unit T maze had been tested previously (14). No significant age difference was observed in [3H]CGS 19755 binding in hippocampi from old Fischer-344 rats (27 months) as compared with mature but not senescent rats (9 months); however, old rats that received chronic treatment with a low dose of nimodipine (20 mg pellets implanted subcutaneously twice during 70 days of treatment) showed higher levels of binding. A high dose of nimodipine (40 mg pellets implanted by the same route and at the same times as the low dose) was without effect on [3H]CGS 19755 binding, although aged rats given this treatment performed better in the maze than rats that received no nimodipine or the low dose. In a second experiment comparing hippocampi of young (4 months) and old (24 months) rats, saturation studies confirmed the lack of an age difference in [3H]CGS 19755 binding. The findings suggest that neither the age-related decline in maze performance nor the enhancement of behavior by nimodipine depend upon changes in hippocampal NMDA receptors.

[Distribution of lipoprotein fractions in men with arteriosclerosis obliterans]. / A lipoprotein frakciók megoszlása arteriosclerosis obliteransban szenvedö férfiakban.

The fasting serum total cholesterol, triglyceride, LDL-cholesterol, VLDL-cholesterol and HDL-cholesterol were determined in fifty male patients with arteriosclerosis obliterans (ASO) confirmed by angiography. Twenty five of the patients were hyperlipidemic and significantly elevated concentration of atherogenic lipoproteins could be demonstrated compared to age matched control group of healthy subjects (n = 20). The HDL-cholesterol level in the patient group was significantly decreased even if comparing normolipemic patients to controls. In the postprandial phase of cholesterol loading (600 mg) the serum total cholesterol, LDL-cholesterol and HDL-cholesterol levels did not change in both groups. A marked increase in serum total triglyceride, VLDL-cholesterol and VLDL/HDL-cholesterol ratio was detected and the differences between the two groups regarding these lipoprotein fractions were increased. The importance of cholesterol-rich VLDL in ASO and its relationship to familial dysbetalipoproteinemia are discussed.