Aging-related increase in hippocampal calcium channels.
This paper briefly reviews more than 10 years of our studies on brain aging and voltage-activated calcium (Ca) currents in rat hippocampal CA1 neurons. Initial studies in the hippocampal slice preparations found that synaptic plasticity was impaired with aging, apparently due to excess Ca influx. In subsequent analyses it was found that the Ca-dependent afterhyperpolarization, the Ca action potential and voltage-activated Ca currents were all increased in aged CA1 neurons. This was not due to impaired inactivation processes. Multiple types of Ca channels appear to be affected by aging. A long Ca tail current was also found in these studies, which seems to represent an unrecognized and significant Ca entry pathway at resting potential. In primary cell cultures, Ca currents and single Ca channels increase steadily over the life cycle of the cultured neurons and are correlated with cell death. Single L-type Ca channels were also studied in brain neurons of an aged mammal (rat), using the partially dissociated ("zipper") hippocampal slice preparation. A substantial increase in the density of functionally available Ca channels was present in CA1 neurons of aged rats, similar to the increase seen in cultured neurons. Thus, a gradual increase in the density of Ca channels appears to be a consistent property of hippocampal neuronal aging and might well be a factor in the vulnerability of aged neurons to Alzheimer's disease and other neurodegenerative/traumatic conditions.
Landfield
P W
PW
Department of Pharmacology, University of Kentucky, Lexington 40536-0084, USA.
D000375:Aging / Q000378:metabolism* / Q000502:physiology; D000818:Animals; D015220:Calcium Channels / Q000378:metabolism*; D006624:Hippocampus / Q000166:cytology / Q000378:metabolism* / Q000502:physiology; D006801:Humans; D015640:Ion Channel Gating; D009474:Neurons / Q000166:cytology / Q000378:metabolism
D015220:Calcium Channels