Medial prefrontal cortex supports accurate source memory retrieval for items encoded under self-reference

2010 ◽  
Author(s):  
Eric D. Leshikar ◽  
Audrey L. Duarte
2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Karuna Subramaniam ◽  
Leighton B. N. Hinkley ◽  
Danielle Mizuiri ◽  
Hardik Kothare ◽  
Chang Cai ◽  
...  

2019 ◽  
Vol 237 (1) ◽  
pp. 231-248 ◽  
Author(s):  
Joachim Latusz ◽  
Marzena Maćkowiak

Abstract Rationale Several findings indicate that early-life dysfunction of N-methyl-d-aspartate (NMDA) receptors might cause schizophrenia-like abnormalities in adulthood that might be induced by impairments in epigenetic regulation. Objectives In the present study, we investigated whether postnatal blockade of NMDA receptors (within the first 3 weeks of life) by the competitive antagonist CGP 37849 (CGP) might affect some epigenetic markers in the adult medial prefrontal cortex (mPFC). Methods Histone H3 phosphorylation at serine 10 (H3S10ph), histone H3 acetylation at lysine 9 or 14 (H3K9ac or H3K14ac, respectively), or expression of histone deacetylase (HDAC) 2, HDAC5, myocyte enhancer factor (MEF) 2D and activity-regulated cytoskeleton-associated protein (Arc) were analysed. Moreover, we also evaluated whether the deacetylase inhibitor sodium butyrate (SB; 1.2 mg/kg, ip) could prevent behavioural and neurochemical changes in the mPFC induced by CGP during memory retrieval in the trace fear conditioning paradigm. Results The results showed that CGP administration increased the number of H3S10ph nuclei but did not affect H3K9ac and H3K14ac or HDAC2 protein levels. However, CGP administration altered the HDAC5 mRNA and protein levels and increased the mRNA and protein levels of MEF2D. CGP also increased Arc mRNA, which was correlated with an increase in the amount of Arc DNA bound to MEF2D. SB given 2 h after training prevented impairment of the freezing response and disruption of epigenetic markers (H3S10ph, HDAC5, MEF2D) and Arc expression during memory retrieval induced by CGP administration. Conclusions The early-life blockade of NMDA receptors impairs some epigenetic regulatory processes in the mPFC that are involved in fear memory formation.


2013 ◽  
Vol 20 (4) ◽  
pp. 201-209 ◽  
Author(s):  
G. J. Peters ◽  
C. N. David ◽  
M. D. Marcus ◽  
D. M. Smith

Hippocampus ◽  
2014 ◽  
Vol 24 (9) ◽  
pp. 1070-1080 ◽  
Author(s):  
Jade Q. Wu ◽  
Greg J. Peters ◽  
Pedro Rittner ◽  
Thomas A. Cleland ◽  
David M. Smith

2021 ◽  
Author(s):  
Camill Burden ◽  
Ryan C. Leach ◽  
Allison M. Sklenar ◽  
Pauline Urban Levy ◽  
Andrea N. Frankenstein ◽  
...  

2006 ◽  
Vol 18 (7) ◽  
pp. 1133-1146 ◽  
Author(s):  
Trudy Y. Kuo ◽  
Cyma Van Petten

The prefrontal cortex is strongly engaged by some, but not all, episodic memory tests. Prior work has shown that source recognition tests—those that require memory for conjunctions of studied attributes—yield deficient performance in patients with prefrontal damage and greater prefrontal activity in healthy subjects, as compared to simple recognition tests. Here, we tested the hypothesis that there is no intrinsic relationship between the prefrontal cortex and source memory, but that the prefrontal cortex is engaged by the demand to retrieve weakly encoded relationships. Subjects attempted to remember object/color conjunctions after an encoding task that focused on object identity alone, and an integrative encoding task that encouraged attention to object/color relationships. After the integrative encoding task, the late prefrontal brain electrical activity that typically occurs in source memory tests was eliminated. Earlier brain electrical activity related to successful recognition of the objects was unaffected by the nature of prior encoding.


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