scholarly journals SGK protein kinase facilitates the expression of long-term potentiation in hippocampal neurons

2006 ◽  
Vol 13 (2) ◽  
pp. 114-118 ◽  
Author(s):  
Y. L. Ma
Keyword(s):  
Protein Kinase ◽  
Hippocampal Neurons ◽  
Long Term Potentiation ◽  
Term Potentiation

Differential effects of protein kinase inhibitors on pre-established long-term potentiation in rat hippocampal neurons in vitro

1991 ◽  
Vol 121 (1-2) ◽  
pp. 259-262 ◽  
Author(s):  
Henry Matthies ◽  
Thomas Behnisch ◽  
Hiroshi Kase ◽  
Hansjürgen Matthies ◽  
Klaus G. Reymann
Keyword(s):  
Protein Kinase ◽  
Hippocampal Neurons ◽  
Kinase Inhibitors ◽  
Long Term Potentiation ◽  
Protein Kinase Inhibitors ◽  
Differential Effects ◽  
Term Potentiation

scholarly journals Soluble Aβ Inhibits Specific Signal Transduction Cascades Common to the Insulin Receptor Pathway

2007 ◽  
Vol 282 (46) ◽  
pp. 33305-33312 ◽  
Author(s):  
Matthew Townsend ◽  
Tapan Mehta ◽  
Dennis J. Selkoe
Keyword(s):  
Protein Kinase ◽  
Alzheimer Disease ◽  
Insulin Receptor ◽  
Hippocampal Neurons ◽  
Amyloid Β ◽  
Principal Component ◽  
Long Term Potentiation ◽  
Amyloid Β Protein ◽  
Term Potentiation

Numerous studies have now shown that the amyloid β-protein (Aβ), the principal component of cerebral plaques in Alzheimer disease, rapidly and potently inhibits certain forms of synaptic plasticity. The amyloid (or Aβ) hypothesis proposes that the continuous disruption of normal synaptic physiology by Aβ contributes to the development of Alzheimer disease. However, there is little consensus about how Aβ mediates this inhibition at the molecular level. Using mouse primary hippocampal neurons, we observed that a brief treatment with cell-derived, soluble, human Aβ disrupted the activation of three kinases (Erk/MAPK, CaMKII, and the phosphatidylinositol 3-kinase-activated protein Akt/protein kinase B) that are required for long term potentiation, whereas two other kinases (protein kinase A and protein kinase C) were stimulated normally. An antagonist of the insulin receptor family of tyrosine kinases was found to mimic the pattern of Aβ-mediated kinase inhibition. We then found that soluble Aβ binds to the insulin receptor and interferes with its insulin-induced autophosphorylation. Taken together, these data demonstrate that physiologically relevant levels of naturally secreted Aβ interfere with insulin receptor function in hippocampal neurons and prevent the rapid activation of specific kinases required for long term potentiation.

Protein kinase C injection into hippocampal pyramidal cells elicits features of long term potentiation

Nature ◽  
1987 ◽  
Vol 328 (6129) ◽  
pp. 426-429 ◽  
Author(s):  
G.-Y. Hu ◽  
Ø. Hvalby ◽  
S. I. Walaas ◽  
K. A. Albert ◽  
P. Skjeflo ◽  
...  
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Pyramidal Cells ◽  
Long Term Potentiation ◽  
Kinase C ◽  
Term Potentiation ◽  
Hippocampal Pyramidal Cells

scholarly journals Selective increase of functional network connectivity in Arc-positive neuronal engrams after long-term potentiation

2020 ◽  
Author(s):  
Yuheng Jiang ◽  
Antonius M.J. VanDongen
Keyword(s):  
Functional Connectivity ◽  
Hippocampal Neurons ◽  
Network Effects ◽  
Network Connectivity ◽  
Long Term Potentiation ◽  
Early Gene ◽  
Memory Traces ◽  
Term Potentiation ◽  
Memory Engram

ABSTRACTNew tools in optogenetics and molecular biology have culminated in recent studies which mark immediate-early gene (IEG)-expressing neurons as memory traces or engrams. Although the activity-dependent expression of IEGs has been successfully utilised to label memory traces, their roles in engram specification is incompletely understood. Outstanding questions remain as to whether expression of IEGs can interplay with network properties such as functional connectivity and also if neurons expressing different IEGs are functionally distinct. We investigated the expression of Arc and c-Fos, two commonly utilised IEGs in memory engram specification, in cultured hippocampal neurons. After pharmacological induction of long-term potentiation (LTP) in the network, we noted an emergent network property of refinement in functional connectivity between neurons, characterized by a global down-regulation of network connectivity, together with strengthening of specific connections. Subsequently, we show that Arc expression correlates with the effects of network refinement, with Arc-positive neurons being selectively strengthened. Arc positive neurons were also found to be located in closer physical proximity to each other in the network. While the expression pattern of IEGs c-Fos and Arc strongly overlaps, Arc was more selectively expressed than c-Fos. These IEGs also act together in coding information about connection strength pruning. These results demonstrate important links between IEG expression and network connectivity, which serve to bridge the gap between cellular correlates and network effects in learning and memory.

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