scholarly journals Role of the somatostatin system in contextual fear memory and hippocampal synaptic plasticity

2008 ◽  
Vol 15 (4) ◽  
pp. 252-260 ◽  
Author(s):  
C. Kluge ◽  
C. Stoppel ◽  
C. Szinyei ◽  
O. Stork ◽  
H.-C. Pape
Keyword(s):  
Synaptic Plasticity ◽  
Fear Memory ◽  
Contextual Fear ◽  
Contextual Fear Memory ◽  
Hippocampal Synaptic Plasticity

scholarly journals The Possible Role of Neurobeachin in Extinction of Contextual Fear Memory

2018 ◽  
Vol 8 (1) ◽  
Author(s):  
Boyoung Lee ◽  
Eunyoung Bang ◽  
Won Suk Yang ◽  
Afshin Paydar ◽  
Go Eun Ha ◽  
...  
Keyword(s):  
Fear Memory ◽  
Contextual Fear ◽  
Contextual Fear Memory

Roles of CREB Signaling Pathway in Regulation of Fear Memory

2009 ◽  
Vol 24 (S1) ◽  
pp. 1-1
Author(s):  
S. Kida
Keyword(s):  
Gene Expression ◽  
Gene Expression Regulation ◽  
Fear Memory ◽  
Brain Regions ◽  
Contextual Fear ◽  
Contextual Fear Memory ◽  
New Gene ◽  
Activity Dependent

Activity-dependent gene expression through activation of Ca2+-CREB signal transduction pathways has been thought to play a central role in fear memory formation. On the other hand, retrieval of fear memory triggers two time-dependent phases of reactivated memory; reconsolidation and extinction. To understand the mechanisms for determining the fate of the reactivated fear memory, we investigated roles of CREB in reconsolidation and extinction of contextual fear memory and then analyzed the brain-regions regulating reconsolidation and extinction by identifying regions where CREB-mediated gene expression is activated and then examining the role of protein synthesis in those regions on reconsolidation and extinction. We first showed that activation of CREB-mediated transcription is required for reconsolidation and long-term extinction of contextual fear memory. Using immunocytochemical analyses, we demonstrated that CREB is activated in the hippocampus/amygdala and amygdala/medial prefrontal cortex (mPFC) in the reconsolidation and extinction phases, respectively. Similar results were observed by analyzing the expression of a CREB-dependent gene, Arc. We finally showed that reconsolidation and long-term extinction of the contextual fear memory depended on new gene expression in the hippocampus/amygdala and amygdala/mPFC, respectively. Thus reactivated contextual fear memory is reconsolidated or extinguished through distinct CREB-mediated gene expression regulation in the hippocampus, amygdala and mPFC.

scholarly journals Adenosine A2A Receptors in the Amygdala Control Synaptic Plasticity and Contextual Fear Memory

2016 ◽  
Vol 41 (12) ◽  
pp. 2862-2871 ◽  
Author(s):  
Ana Patrícia Simões ◽  
Nuno J Machado ◽  
Nélio Gonçalves ◽  
Manuella P Kaster ◽  
Ana T Simões ◽  
...  
Keyword(s):  
Synaptic Plasticity ◽  
Fear Memory ◽  
Adenosine A2a Receptors ◽  
Contextual Fear ◽  
Contextual Fear Memory ◽  
A2a Receptors ◽  
Adenosine A2a

scholarly journals Lentiviral silencing of GSK-3β in adult dentate gyrus impairs contextual fear memory and synaptic plasticity

2015 ◽  
Vol 9 ◽  
Author(s):  
Benjamin Chew ◽  
Jae Ryun Ryu ◽  
Teclise Ng ◽  
Dongliang Ma ◽  
Ananya Dasgupta ◽  
...  
Keyword(s):  
Synaptic Plasticity ◽  
Dentate Gyrus ◽  
Fear Memory ◽  
Contextual Fear ◽  
Contextual Fear Memory ◽  
Gsk 3Β

scholarly journals Contextual Fear Memory Maintenance Changes Expression of pMAPK, BDNF and IBA-1 in the Pre-limbic Cortex in a Layer-Specific Manner

2021 ◽  
Vol 15 ◽  
Author(s):  
Nicholas Chaaya ◽  
Joshua Wang ◽  
Angela Jacques ◽  
Kate Beecher ◽  
Michael Chaaya ◽  
...  
Keyword(s):  
Fear Conditioning ◽  
Fear Memory ◽  
Contextual Fear Conditioning ◽  
Mitogen Activated Protein Kinase ◽  
Limbic Cortex ◽  
Pavlovian Fear Conditioning ◽  
Bdnf Expression ◽  
Contextual Fear ◽  
Contextual Fear Memory

Post-traumatic stress disorder (PTSD) is a debilitating and chronic fear-based disorder. Pavlovian fear conditioning protocols have long been utilised to manipulate and study these fear-based disorders. Contextual fear conditioning (CFC) is a particular Pavlovian conditioning procedure that pairs fear with a particular context. Studies on the neural mechanisms underlying the development of contextual fear memories have identified the medial prefrontal cortex (mPFC), or more specifically, the pre-limbic cortex (PL) of the mPFC as essential for the expression of contextual fear. Despite this, little research has explored the role of the PL in contextual fear memory maintenance or examined the role of neuronal mitogen-activated protein kinase (pMAPK; ERK 1/2), brain-derived neurotrophic factor (BDNF), and IBA-1 in microglia in the PL as a function of Pavlovian fear conditioning. The current study was designed to evaluate how the maintenance of two different long-term contextual fear memories leads to changes in the number of immune-positive cells for two well-known markers of neural activity (phosphorylation of MAPK and BDNF) and microglia (IBA-1). Therefore, the current experiment is designed to assess the number of immune-positive pMAPK and BDNF cells, microglial number, and morphology in the PL following CFC. Specifically, 2 weeks following conditioning, pMAPK, BDNF, and microglia number and morphology were evaluated using well-validated antibodies and immunohistochemistry (n = 12 rats per group). A standard CFC protocol applied to rats led to increases in pMAPK, BDNF expression and microglia number as compared to control conditions. Rats in the unpaired fear conditioning (UFC) procedure, despite having equivalent levels of fear to context, did not have any change in pMAPK, BDNF expression and microglia number in the PL compared to the control conditions. These data suggest that alterations in the expression of pMAPK, BDNF, and microglia in the PL can occur for up to 2 weeks following CFC. Together the data suggest that MAPK, BDNF, and microglia within the PL of the mPFC may play a role in contextual fear memory maintenance.

scholarly journals Molecular motor KIF3B in the prelimbic cortex constrains the consolidation of contextual fear memory

2021 ◽  
Vol 14 (1) ◽  
Author(s):  
Nadine F. Joseph ◽  
Aya Zucca ◽  
Jenna L. Wingfield ◽  
Isabel Espadas ◽  
Damon Page ◽  
...  
Keyword(s):  
Molecular Motor ◽  
Fear Memory ◽  
Contextual Fear Conditioning ◽  
Prelimbic Cortex ◽  
Spine Density ◽  
Cellular Mechanisms ◽  
Contextual Fear ◽  
Contextual Fear Memory ◽  
And Function

AbstractMolecular and cellular mechanisms underlying the role of the prelimbic cortex in contextual fear memory remain elusive. Here we examined the kinesin family of molecular motor proteins (KIFs) in the prelimbic cortex for their role in mediating contextual fear, a form of associative memory. KIFs function as critical mediators of synaptic transmission and plasticity by their ability to modulate microtubule function and transport of gene products. However, the regulation and function of KIFs in the prelimbic cortex insofar as mediating memory consolidation is not known. We find that within one hour of contextual fear conditioning, the expression of KIF3B is upregulated in the prelimbic but not the infralimbic cortex. Importantly, lentiviral-mediated knockdown of KIF3B in the prelimbic cortex produces deficits in consolidation while reducing freezing behavior during extinction of contextual fear. We also find that the depletion of KIF3B increases spine density within prelimbic neurons. Taken together, these results illuminate a key role for KIF3B in the prelimbic cortex as far as mediating contextual fear memory.

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