Effect of age on blood vessels and neurovascular appositions in the CA1 region of the rat hippocampus.

Rats aged 3, 9, 24 and 30 months were used in this study. Increased basal lamina thickening in capillaries, muscular large vessels and nonmuscular large vessels was shown with advancing age. There is also an age-related increase in the area of mitochondria in smooth muscle cells. These ultrastructural changes may underlie observed age-related functional changes in the vasculature. They may be a compensatory response of the vessel wall cells to a declining capacity to handle the continual and varying shear stress exerted by the blood. Ultrastructural differences between capillaries and the two types of large vessels are reported and discussed in terms of their functional significance. It was noted that there are more dendrites adjacent to capillaries than to large vessels, however, this was unaffected by increasing age. Since advancing age did not alter the number of neuronal processes adjacent to vessels, age-related compromises in vessel function may not be subjected to neuronal regulation.

Effect of age on blood vessels and neurovascular appositions in the rat dentate fascia.

Rats aged 3, 9, 24 and 30 months were used in this study. We show increased basal lamina thickening and increased mitochondrial presence in walls of capillaries and not in walls of large vessel populations with age. This suggests that age selectively affects capillary structure. Ultrastructural differences between capillaries and two types of large vessels are reported and discussed in terms of their probable functional significance. In particular it was noted that there are more axon terminals, axons and dendrites adjacent to capillaries than to large vessels and that this was unaffected by increasing age. It is not clear whether the proximity of neuronal processes to a vessel wall serves a function, however, the larger number adjacent to capillaries than to large vessels indicates a more significant role for them in capillary rather than in large vessel function. Since increasing age did not alter the number of neuronal processes adjacent to vessels, age-related compromises in vessel function may be unrelated to neuronal regulation. The age-related changes are discussed as possible vascular markers for the aging brain.

Nuclear pore complex frequency in CA1 pyramidal cells of the aging rat.

The frequency and the diameter of nuclear pore complexes, and the nuclear perimeter, were studied in CA1 pyramidal cells of the hippocampi from 3-, 9-, 24-, and 30-month-old rats (Fischer 344). No changes with age in any of these parameters were observed. This finding is discussed in terms of varied responses of different brain areas to the effects of aging.

Changes in the nuclear pore complexes of the dentate granule cells in aged rats.

In 3-, 9-, 24-, and 30-month-old male rats (Fischer 344), the nuclear perimeter and the density and diameter of nuclear pore complexes in the granule cells of the dentate fascia were studied. Whereas the nuclear perimeter and the diameter of nuclear pore complexes did not change as a function of age, there was a significant loss of them at 24 months (20%), compared with the third month. This change suggests that the nucleocytoplasmic communication may be impaired with age which would adversely affect protein synthesis, and could explain the loss of the postsynaptic sites of the dentate fascia of aged rats.

Calcium distribution in dendritic spines of the dentate fascia varies with age.

Calcium distribution in dendritic spines of the dentate fascia was studied as a function of age with the oxalate-pyroantimonate precipitation technique. In postnatal ages P3, P9, P24 and P30 spines were analyzed as to the presence of the spine apparatus (SA) and as to the presence of Ca2+ deposits within the SA and within the spine cytoplasm. The percentage of spines with SA-containing precipitates declined significantly between P3 and P24. Conversely, the percentage of spines with precipitates in the spine cytoplasm was significantly increased by P24. In the absence of an SA loss, this result suggests an age-related decrease in the Ca2+-sequestering capacity by the SA. These parameters were improved by P30 so that they approximated the values of P3. Such a seeming amelioration could be attributed to the fact that the mortality rate in rats sharply increases by P24, so that animals surviving this age represent a selected population in which a compensatory growth of spines has occurred and has secured functionally valid connections.