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ARS Home » Northeast Area » Boston, Massachusetts » Jean Mayer Human Nutrition Research Center On Aging » Research » Publications at this Location » Publication #184331
Title: BLUEBERRY EXTRACT INHIBITS DA-OR AB-INDUCED DECREMENTS IN CALCIUM FLUX IN PRIMARY HIPPOCAMPAL CELLS

Author
item Joseph, James
item Fisher, Derek

Submitted to: Society for Neuroscience Abstracts and Proceedings
Publication Type: Abstract Only
Publication Acceptance Date: 7/15/2005
Publication Date: 11/12/2005
Citation: Joseph, J.A., Fisher, D.R. 2005. Blueberry extract inhibits da-or ab-induced decrements in calcium flux in primary hippocampal cells. Society for Neuroscience Abstracts and Proceedings. Abstract No. 93.6.

Interpretive Summary: NOT NEEDED

Technical Abstract: Previously, we have shown that when exposed to dopamine (DA) or amyloid beta (A') COS-7 cells transfected with muscarinic receptor (MAChR) subtypes (M1, M2, or M4) lose their ability to buffer or extrude calcium following oxotremorine-induced depolarization. However, pre-treatment of these cells with a high antioxidant blueberry extract (BB) prevented the DA or A' effects on calcium buffering. Similarly, it also appears that dietary BB also reversed several parameters of neuronal and behavioral aging in rodents, including cognitive function. It has been postulated that at least part of the loss of cognitive function in aging may dependent upon a dysregulation in calcium homeostasis, and this loss affects numerous downstream signaling pathways that could ultimately affect learning and memory. Present experiments were carried out to determine the role of oxidative stress in this calcium regulation by assessing whether: a) calcium buffering would be altered in DA- or A'-exposed cultured primary hippocampal neuronal cells (HNC) and b) BB or BB polyphenolic pretreatment of the cells would prevent these deficits. Thus, control or BB (0.5mg/ml)-treated HNC were exposed to 0, 0.1mM DA or 100'M A' and Ca2+ buffering (Ca2+ recovery time, Ca2+RT, following KCl) was then carried out on the cells prior to and following the KCl-induced depolarization. Ca2+RT was assessed as the % of HNC showing recovery to 50% -70% of control at 5, 10, or 15 min after depolarization. Results indicated that DA significantly lowered Ca2+RT in the HNC at all times examined after depolarization. However, BB-treatment prevented these declines to 50%-60% of control, especially at the 10 and 15 min post depolarization. Thus far, A' 25-35 effects were similar to those seen using DA, with BB pre-treatment preventing A'-induced deficits in calcium buffering. Results will be discussed in terms of previous findings showing BB supplementation in senescent rats enhanced memory and MAPk signaling.