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.

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.

PKMζ maintains remote contextual fear memory by inhibiting GluA2-dependent AMPA receptor endocytosis in the prelimbic cortex

Neuroscience ◽  
2021 ◽  
Author(s):  
Lucas A. Marcondes ◽  
Jociane de C. Myskiw ◽  
Eduarda G. Nachtigall ◽  
Rodrigo F. Narvaes ◽  
Ivan Izquierdo ◽  
...  
Keyword(s):  
Ampa Receptor ◽  
Fear Memory ◽  
Prelimbic Cortex ◽  
Contextual Fear ◽  
Contextual Fear Memory ◽  
Receptor Endocytosis

scholarly journals Encoding of Contextual Fear Memory Requires De Novo Proteins in the Prelimbic Cortex

2017 ◽  
Vol 2 (2) ◽  
pp. 158-169 ◽  
Author(s):  
Valerio Rizzo ◽  
Khalid Touzani ◽  
Bindu L. Raveendra ◽  
Supriya Swarnkar ◽  
Joan Lora ◽  
...  
Keyword(s):  
De Novo ◽  
Fear Memory ◽  
Prelimbic Cortex ◽  
Contextual Fear ◽  
Contextual Fear Memory ◽  
De Novo Proteins

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

scholarly journals Neurogenesis-induced forgetting is associated with reduced neuronal activity in CA1 during context fear memory retrieval

2021 ◽  
Author(s):  
Alexandria Evans ◽  
Gavin A. Scott ◽  
Jonathan R. Epp
Keyword(s):  
Memory Retrieval ◽  
Wheel Running ◽  
Fear Memory ◽  
Hippocampal Neurogenesis ◽  
Contextual Fear Conditioning ◽  
Early Gene ◽  
Population Activity ◽  
Contextual Fear ◽  
Induced Forgetting

AbstractHippocampal neurogenesis has a role in many essential learning and memory processes, including forgetting. This forgetting process is important because it prevents proactive interference between old and new memories. While several studies have now established the role of neurogenesis in forgetting, the specific mechanisms mediating neurogenesis-induced forgetting have not been elucidated. The goal of this study was to examine how increased neurogenesis affects the recall of context fear memory in addition to its effects on population activity within hippocampal subregions. We trained mice in contextual fear conditioning and then increased neurogenesis via 4 weeks of voluntary wheel running. Increased neurogenesis led to a reduction in freezing behaviour during context testing, replicating previous studies showing that increased neurogenesis causes forgetting of context fear memories. Additionally, we mapped the expression of the immediate early gene c-Fos within hippocampal subregions and found that increasing neurogenesis led to reduced CA1 c-Fos expression during context testing. The results suggest that reduced CA1 population activity may underlie the association between increased neurogenesis and forgetting.

scholarly journals Parvalbumin-positive interneurons mediate neocortical-hippocampal interactions that are necessary for memory consolidation

eLife ◽  
2017 ◽  
Vol 6 ◽  
Author(s):  
Frances Xia ◽  
Blake A Richards ◽  
Matthew M Tran ◽  
Sheena A Josselyn ◽  
Kaori Takehara-Nishiuchi ◽  
...  
Keyword(s):  
Prefrontal Cortex ◽  
Fear Conditioning ◽  
Medial Prefrontal Cortex ◽  
Memory Consolidation ◽  
Fear Memory ◽  
Contextual Fear Conditioning ◽  
Contextual Fear ◽  
Contextual Fear Memory ◽  
Spiking Activity

Following learning, increased coupling between spindle oscillations in the medial prefrontal cortex (mPFC) and ripple oscillations in the hippocampus is thought to underlie memory consolidation. However, whether learning-induced increases in ripple-spindle coupling are necessary for successful memory consolidation has not been tested directly. In order to decouple ripple-spindle oscillations, here we chemogenetically inhibited parvalbumin-positive (PV+) interneurons, since their activity is important for regulating the timing of spiking activity during oscillations. We found that contextual fear conditioning increased ripple-spindle coupling in mice. However, inhibition of PV+ cells in either CA1 or mPFC eliminated this learning-induced increase in ripple-spindle coupling without affecting ripple or spindle incidence. Consistent with the hypothesized importance of ripple-spindle coupling in memory consolidation, post-training inhibition of PV+ cells disrupted contextual fear memory consolidation. These results indicate that successful memory consolidation requires coherent hippocampal-neocortical communication mediated by PV+ cells.

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