scholarly journals CREB Activation Mediates Plasticity in Cultured Hippocampal Neurons

1998 ◽  
Vol 6 (3) ◽  
pp. 1-7 ◽  
Author(s):  
Menahem Segal ◽  
Diane D. Murphy
Keyword(s):  
Cyclic Amp ◽  
Dendritic Spines ◽  
Hippocampal Neurons ◽  
Long Term Potentiation ◽  
Spine Density ◽  
Creb Phosphorylation ◽  
Molecular Events ◽  
Term Potentiation ◽  
Element Binding Protein ◽  
Responsive Element

Activation of cyclic AMP dependent kinase is believed to mediate slow onset, long-term potentiation (LTP) in central neurons. Cyclic- AMP activates a cascade of molecular events leading to phosphorylation of the nuclear cAMP responsive element binding protein (pCREB). Whereas a variety of stimuli lead to activation of CREB, the molecular processes downstream of CREB, which may be relevant to neuronal plasticity, are yet largely unknown. We have recently found that following exposure to estradiol, pCREB mediates the large increase in dendritic spine density in cultured rat hippocampal neurons. We now extend these observations to include other stimuli, such as bicuculline, that cause the formation of new dendritic spines. Such stimuli share with estradiol the same mechanism of action in that both require activity-dependent CREB phosphorylation. Our observations suggest that CREB phosphorylation is a necessary, but perhaps not sufficient, step in the process leading to the generation of new dendritic spines and perhaps to functional plasticity as well.

scholarly journals Chemical LTD, but not LTP, induces transient accumulation of gelsolin in dendritic spines

2019 ◽  
Vol 400 (9) ◽  
pp. 1129-1139 ◽  
Author(s):  
Iryna Hlushchenko ◽  
Pirta Hotulainen
Keyword(s):  
Synaptic Plasticity ◽  
Dendritic Spines ◽  
Hippocampal Neurons ◽  
Long Term Potentiation ◽  
Excitatory Synapses ◽  
Signal Molecule ◽  
Brain Functions ◽  
Dendritic Shaft ◽  
Term Potentiation

Abstract Synaptic plasticity underlies central brain functions, such as learning. Ca2+ signaling is involved in both strengthening and weakening of synapses, but it is still unclear how one signal molecule can induce two opposite outcomes. By identifying molecules, which can distinguish between signaling leading to weakening or strengthening, we can improve our understanding of how synaptic plasticity is regulated. Here, we tested gelsolin’s response to the induction of chemical long-term potentiation (cLTP) or long-term depression (cLTD) in cultured rat hippocampal neurons. We show that gelsolin relocates from the dendritic shaft to dendritic spines upon cLTD induction while it did not show any relocalization upon cLTP induction. Dendritic spines are small actin-rich protrusions on dendrites, where LTD/LTP-responsive excitatory synapses are located. We propose that the LTD-induced modest – but relatively long-lasting – elevation of Ca2+ concentration increases the affinity of gelsolin to F-actin. As F-actin is enriched in dendritic spines, it is probable that increased affinity to F-actin induces the relocalization of gelsolin.

scholarly journals Protein Kinases Mediate Increment of the Phosphorylation of Cyclic AMP -Responsive Element Binding Protein in Spinal Cord of Rats following Capsaicin Injection

2005 ◽  
Vol 1 ◽  
pp. 1744-8069-1-26 ◽  
Author(s):  
Jing Wu ◽  
Guangxiao Su ◽  
Long Ma ◽  
Xuan Zhang ◽  
Yongzhong Lei ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Cyclic Amp ◽  
Protein Kinases ◽  
Binding Protein ◽  
Cellular Membrane ◽  
Creb Phosphorylation ◽  
Nociceptive Neurons ◽  
Mitogen Activated Protein ◽  
Element Binding Protein ◽  
Responsive Element

Background: Strong noxious stimuli cause plastic changes in spinal nociceptive neurons. Intracellular signal transduction pathways from cellular membrane to nucleus, which may further regulate gene expression by critical transcription factors, convey peripheral stimulation. Cyclic AMP-responsive element binding protein (CREB) is a well-characterized stimulus-induced transcription factor whose activation requires phosphorylation of the Serine-133 residue. Phospho-CREB can further induce gene transcription and strengthen synaptic transmission by the activation of the protein kinase cascades. However, little is known about the mechanisms by which CREB phosphorylation is regulated by protein kinases during nociception. This study was designed to use Western blot analysis to investigate the role of mitogen-activated protein (MAP)/extracellular signal-regulated kinase (ERK) kinase (MEK 1/2), PKA and PKC in regulating the phosphorylation of CREB in the spinal cord of rats following intraplantar capsaicin injection. Results: We found that capsaicin injection significantly increased the phosphorylation level of CREB in the ipsilateral side of the spinal cord. Pharmacological manipulation of MEK 1/2, PKA and PKC with their inhibitors (U0126, H89 and NPC 15473, respectively) significantly blocked this increment of CREB phosphorylation. However, the expression of CREB itself showed no change in any group. Conclusion: These findings suggest that the activation of intracellular MAP kinase, PKA and PKC cascades may contribute to the regulation of phospho-CREB in central nociceptive neurons following peripheral painful stimuli.

scholarly journals Sensitivity of Synaptic Plasticity to the Ca2+ Permeability of NMDA Channels: A Model of Long-Term Potentiation in Hippocampal Neurons

1993 ◽  
Vol 5 (5) ◽  
pp. 681-694 ◽  
Author(s):  
Erik De Schutter ◽  
James M. Bower
Keyword(s):  
Nmda Receptor ◽  
Dendritic Spines ◽  
Hippocampal Neurons ◽  
Dendritic Tree ◽  
Long Term Potentiation ◽  
Synaptic Activation ◽  
Term Potentiation ◽  
Nmda Channels ◽  
Maximum Amplification

We have examined a model by Holmes and Levy (1990) of the induction of associative long-term potentiation (LTP) by a rise in the free Ca2+ concentration ([Ca2+]) after synaptic activation of dendritic spines. The previously reported amplification of the change in [Ca2+] caused by coactivation of several synapses was found to be quite sensitive to changes in the permeability of the N-methyl-D-aspartate (NMDA) receptor channels to Ca2+. Varying this parameter indicated that maximum amplification is obtained at values that are close to Ca2+ permeabilities reported in the literature. However, amplification failed if permeability is reduced by more than 50%. We also found that the maximum free [Ca2+] reached in an individual spine during synaptic coactivation of several spines depended on the location of that spine on the dendritic tree. Distal spines attained a higher [Ca2+] than proximal ones, with differences of up to 80%. The implications of this result for the uniformity of induction of associative LTP in spines in different regions of the dendrite are discussed.

scholarly journals Cleavage of cyclic AMP-responsive element-binding protein H aggravates myocardial hypoxia reperfusion injury in a hepatocyte–myocardial cell co-culture system

2020 ◽  
Vol 48 (5) ◽  
pp. 030006052090483
Author(s):  
Zehao Jin ◽  
Ye Chen ◽  
Xiaochun Weng ◽  
Anwu Huang ◽  
Shuang Lin ◽  
...  
Keyword(s):  
Cyclic Amp ◽  
Myocardial Ischemia ◽  
Reperfusion Injury ◽  
Acute Phase ◽  
Proinflammatory Cytokines ◽  
Acute Phase Response ◽  
Culture System ◽  
Element Binding Protein ◽  
Myocardial Hypoxia ◽  
Responsive Element

Objective This study aimed to determine whether proinflammatory cytokines have an effect on myocardial cells (MCs) and hepatocytes during myocardial ischemia to induce cyclic AMP-responsive element-binding protein H (CREBH) cleavage, activate the acute phase response in the liver, and cause a superimposed injury in MCs. Methods In this study, a hepatocyte–MC transwell co-culture system was used to investigate the relationship between myocardial hypoxia/reperfusion injury and CREBH cleavage. MCs and hepatocytes of neonatal rats were obtained from the ventricles and livers of Sprague–Dawley rats, respectively. MCs were inoculated into the lower chamber of transwell chambers for 12 hours under hypoxia. Levels of the endoplasmic reticulum stress protein glucose-regulated protein 78 in MCs, CREBH in hepatocytes, inflammatory factor (tumor necrosis factor-α and interleukin-6) levels, and cell viability were evaluated. The effect of CREBH knockdown was also studied using a CREBH-specific short hairpin RNA (Ad-CREBHi). Results We found that proinflammatory cytokines affect MCs and hepatocytes during myocardial ischemia to induce CREBH cleavage, activate the acute phase response in the liver, and cause superimposed injury in MCs. Conclusions Expression of CREBH aggravates myocardial injury during myocardial ischemia.

scholarly journals Long-Term Potentiation in Isolated Dendritic Spines

PLoS ONE ◽  
2009 ◽  
Vol 4 (6) ◽  
pp. e6021 ◽  
Author(s):  
Amadou T. Corera ◽  
Guy Doucet ◽  
Edward A. Fon
Keyword(s):  
Dendritic Spines ◽  
Long Term Potentiation ◽  
Term Potentiation

Acute cocaine exposure alters spine density and long-term potentiation in the ventral tegmental area

2007 ◽  
Vol 26 (3) ◽  
pp. 749-756 ◽  
Author(s):  
Federica Sarti ◽  
Stephanie L. Borgland ◽  
Viktor N. Kharazia ◽  
Antonello Bonci
Keyword(s):  
Ventral Tegmental Area ◽  
Long Term Potentiation ◽  
Spine Density ◽  
Cocaine Exposure ◽  
Term Potentiation ◽  
Ventral Tegmental
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