BB and hippocampus
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BLUEBERRY EXTRACT INHIBITS DA-OR A-INDUCED DECREMENTS IN CALCIUM FLUX IN PRIMARY HIPPOCAMPAL CELLS
J.A.Joseph*; D.R.Fisher
1. Human Nutrit. Res. Center on Aging, 2. Neuroscience, Tufts Univ., Boston, MA, USA
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/anti-inflammatory 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 be 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 100M 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 1"
BLUEBERRY EXTRACT INHIBITS DA-OR A-INDUCED DECREMENTS IN CALCIUM FLUX IN PRIMARY HIPPOCAMPAL CELLS
J.A.Joseph*; D.R.Fisher
1. Human Nutrit. Res. Center on Aging, 2. Neuroscience, Tufts Univ., Boston, MA, USA
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/anti-inflammatory 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 be 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 100M 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 1"
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