scholarly journals Reversal of Cocaine-Associated Synaptic Plasticity in Medial Prefrontal Cortex Parallels Elimination of Memory Retrieval

2017 ◽  
Vol 42 (10) ◽  
pp. 2000-2010 ◽  
Author(s):  
James M Otis ◽  
Devin Mueller
Keyword(s):  
Prefrontal Cortex ◽  
Synaptic Plasticity ◽  
Medial Prefrontal Cortex ◽  
Memory Retrieval

Decreased synaptic plasticity in the medial prefrontal cortex underlies short-term memory deficits in 6-OHDA-lesioned rats

2016 ◽  
Vol 301 ◽  
pp. 43-54 ◽  
Author(s):  
Filipe C. Matheus ◽  
Daniel Rial ◽  
Joana I. Real ◽  
Cristina Lemos ◽  
Juliana Ben ◽  
...  
Keyword(s):  
Prefrontal Cortex ◽  
Synaptic Plasticity ◽  
Medial Prefrontal Cortex ◽  
Short Term Memory ◽  
Memory Deficits ◽  
Short Term ◽  
Term Memory

Changes in synaptic plasticity in the rat hippocampo-medial prefrontal cortex pathway induced by repeated treatments with fluvoxamine

2002 ◽  
Vol 949 (1-2) ◽  
pp. 131-138 ◽  
Author(s):  
Satoshi Ohashi ◽  
Machiko Matsumoto ◽  
Hiroshi Otani ◽  
Kiyoshi Mori ◽  
Hiroko Togashi ◽  
...  
Keyword(s):  
Prefrontal Cortex ◽  
Synaptic Plasticity ◽  
Medial Prefrontal Cortex

scholarly journals Early-life blockade of NMDA receptors induces epigenetic abnormalities in the adult medial prefrontal cortex: possible involvement in memory impairment in trace fear conditioning

2019 ◽  
Vol 237 (1) ◽  
pp. 231-248 ◽  
Author(s):  
Joachim Latusz ◽  
Marzena Maćkowiak
Keyword(s):  
Prefrontal Cortex ◽  
Nmda Receptors ◽  
Fear Conditioning ◽  
Medial Prefrontal Cortex ◽  
Memory Retrieval ◽  
Early Life ◽  
Histone H3 ◽  
Protein Levels ◽  
Trace Fear Conditioning ◽  
Trace Fear

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.

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