Nerve growth factor inhibits the expression of long-term potentiation in hippocampal slices

Neuroreport ◽  
1993 ◽  
Vol 4 (2) ◽  
pp. 147-150 ◽  
Author(s):  
V. Tancredi ◽  
G. DʼArcangelo ◽  
D. Mercanti ◽  
P. Calissano
Keyword(s):  
Nerve Growth Factor ◽  
Growth Factor ◽  
Hippocampal Slices ◽  
Long Term Potentiation ◽  
Nerve Growth ◽  
Term Potentiation

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
Keyword(s):  
Nerve Growth Factor ◽  
Growth Factor ◽  
Beta Amyloid ◽  
Long Term Potentiation ◽  
Rat Hippocampus ◽  
Nerve Growth ◽  
Term Potentiation

scholarly journals Nerve growth factor favours long-term depression over long-term potentiation in layer II-III neurones of rat visual cortex

2004 ◽  
Vol 559 (2) ◽  
pp. 497-506 ◽  
Author(s):  
Alfredo Brancucci ◽  
Nicola Kuczewski ◽  
Sonia Covaceuszach ◽  
Antonino Cattaneo ◽  
Luciano Domenici
Keyword(s):  
Visual Cortex ◽  
Nerve Growth Factor ◽  
Growth Factor ◽  
Long Term Potentiation ◽  
Long Term Depression ◽  
Nerve Growth ◽  
Term Potentiation

Voltage-Sensitive Calcium Currents Are Acutely Increased by Nerve Growth Factor in PC12 Cells

1999 ◽  
Vol 82 (6) ◽  
pp. 2847-2852 ◽  
Author(s):  
Min Jia ◽  
Minxu Li ◽  
Xu-Wen Liu ◽  
Hao Jiang ◽  
Phillip G. Nelson ◽  
...  
Keyword(s):  
Nerve Growth Factor ◽  
Growth Factor ◽  
Pc12 Cells ◽  
Calcium Current ◽  
Calcium Uptake ◽  
Growth Factor Receptor ◽  
Long Term Potentiation ◽  
Calcium Currents ◽  
Nerve Growth

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.

scholarly journals Involvement of Bradykinin Receptor 2 in Nerve Growth Factor Neuroprotective Activity

Cells ◽  
2020 ◽  
Vol 9 (12) ◽  
pp. 2651
Author(s):  
Carla Petrella ◽  
Maria Teresa Ciotti ◽  
Robert Nisticò ◽  
Sonia Piccinin ◽  
Pietro Calissano ◽  
...  
Keyword(s):  
Nerve Growth Factor ◽  
Growth Factor ◽  
Mechanism Of Action ◽  
Hippocampal Slices ◽  
Primary Cultures ◽  
Long Term Potentiation ◽  
Neuroprotective Activity ◽  
Nerve Growth ◽  
Bradykinin Receptor

Neurotrophin nerve growth factor (NGF) has been demonstrated to upregulate the gene expression of bradykinin receptor 2 (B2R) on sensory neurons, thus facilitating nociceptive signals. The aim of the present study is to investigate the involvement of B2R in the NGF mechanism of action in nonsensory neurons in vitro by using rat mixed cortical primary cultures (CNs) and mouse hippocampal slices, and in vivo in Alzheimer’s disease (AD) transgenic mice (5xFAD) chronically treated with NGF. A significant NGF-mediated upregulation of B2R was demonstrated by microarray, Western blot, and immunofluorescence analysis in CNs, indicating microglial cells as the target of this modulation. The B2R involvement in the NGF mechanism of action was also demonstrated by using a selective B2R antagonist which was able to reverse the neuroprotective effect of NGF in CNs, as revealed by viability assay, and the NGF-induced long-term potentiation (LTP) in hippocampal slices. To confirm in vitro observations, B2R upregulation was observed in 5xFAD mouse brain following chronic intranasal NGF treatment. This study demonstrates for the first time that B2R is a key element in the neuroprotective activity and synaptic plasticity mediated by NGF in brain cells.

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