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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.<\/jats:p>\n              <\/jats:sec><jats:sec>\n                <jats:title>Results<\/jats:title>\n                <jats:p>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.<\/jats:p>\n              <\/jats:sec><jats:sec>\n                <jats:title>Conclusions<\/jats:title>\n                <jats:p>The early-life blockade of NMDA receptors impairs some epigenetic regulatory processes in the mPFC that are involved in fear memory formation.<\/jats:p>\n              <\/jats:sec>","DOI":"10.1007\/s00213-019-05362-5","type":"journal-article","created":{"date-parts":[[2019,10,26]],"date-time":"2019-10-26T00:03:18Z","timestamp":1572048198000},"page":"231-248","update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":15,"title":["Early-life blockade of NMDA receptors induces epigenetic abnormalities in the adult medial prefrontal cortex: possible involvement in memory impairment in trace fear conditioning"],"prefix":"10.1007","volume":"237","author":[{"given":"Joachim","family":"Latusz","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-6056-9595","authenticated-orcid":false,"given":"Marzena","family":"Ma\u0107kowiak","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2019,10,25]]},"reference":[{"key":"5362_CR1","doi-asserted-by":"publisher","first-page":"9","DOI":"10.1093\/schbul\/sbr133","volume":"38","author":"A Adell","year":"2012","unstructured":"Adell A, Jimenez-Sanchez L, Lopez-Gil X, Romon T (2012) Is the acute NMDA receptor hypofunction a valid model of schizophrenia? 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