Lentiviral-mediated overexpression of nerve growth factor (NGF) prevents beta-amyloid [25–35]-induced long term potentiation (LTP) decline in the rat hippocampus

2015 ◽  
Vol 1624 ◽  
pp. 398-404 ◽  
Author(s):  
Shukhrat S. Uzakov ◽  
Andrey D. Ivanov ◽  
Sergey V. Salozhin ◽  
Vladimir A. Markevich ◽  
Natalia V. Gulyaeva
Neuroreport ◽  
1993 ◽  
Vol 4 (2) ◽  
pp. 147-150 ◽  
Author(s):  
V. Tancredi ◽  
G. DʼArcangelo ◽  
D. Mercanti ◽  
P. Calissano

2004 ◽  
Vol 559 (2) ◽  
pp. 497-506 ◽  
Author(s):  
Alfredo Brancucci ◽  
Nicola Kuczewski ◽  
Sonia Covaceuszach ◽  
Antonino Cattaneo ◽  
Luciano Domenici

1999 ◽  
Vol 82 (6) ◽  
pp. 2847-2852 ◽  
Author(s):  
Min Jia ◽  
Minxu Li ◽  
Xu-Wen Liu ◽  
Hao Jiang ◽  
Phillip G. Nelson ◽  
...  

Whole cell calcium currents were recorded from PC12 cells with the perforated patch technique. Currents were evoked by step depolarization from a holding potential of −90 mV. Nerve growth factor (NGF) increased calcium currents through L-type calcium channels by >75% within 3–5 min. This increase was inhibited by K-252a, by nifedipine, and by inhibition or down-regulation of kinase C. Brain-derived neurotrophic factor (BDNF) also increased calcium current, but to a smaller extent. Thus increases in calcium current can be linked to activation of either the high- or the low-affinity nerve growth factor receptor. Increases in presynaptic calcium uptake appear to be a crucial element in the short-term actions of the neurotrophins on neurotransmitter release leading to long-term potentiation. Also, the control of calcium uptake is likely to be an important factor in the long-term actions of the neurotrophins on neuronal survival and neuronal protection. The present data indicate that the PC12 cell may be a useful model for studying the effect of the neurotrophins on calcium uptake.


2012 ◽  
Vol 32 (48) ◽  
pp. 17401-17406 ◽  
Author(s):  
R. Kimura ◽  
D. MacTavish ◽  
J. Yang ◽  
D. Westaway ◽  
J. H. Jhamandas

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