The methylazoxymethanol acetate rat model: molecular and epigenetic effect in the developing prefrontal cortex: An Editorial Highlight for 'Epigenetic mechanisms underlying NMDA receptor hypofunction in the prefrontal cortex of juvenile animals in the MAM model for schizophrenia' on page 320

J Neurochem. 2017 Nov;143(3):264-267. doi: 10.1111/jnc.14133. Epub 2017 Sep 5.


This Editorial highlights an article by Gulchina and colleagues in the current issue of the Journal of Neurochemistry, in which the authors describe molecular and epigenetic changes in the developing prefrontal cortex of the rats exposed to methylazoxymethanol acetate (MAM). They found an NMDAR hypofunction present in the prefrontal cortex of juvenile MAM rats which was associated with abnormal epigenetic regulation of the Grin2b gene. These changes may be related to early cognitive impairments observed in MAM rats and schizophrenia patients.

Publication types

  • Editorial
  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Disease Models, Animal
  • Epigenesis, Genetic / drug effects*
  • Female
  • Methylazoxymethanol Acetate / toxicity*
  • Neurotoxins / toxicity*
  • Prefrontal Cortex* / drug effects
  • Prefrontal Cortex* / growth & development
  • Prefrontal Cortex* / metabolism
  • Pregnancy
  • Prenatal Exposure Delayed Effects* / chemically induced
  • Prenatal Exposure Delayed Effects* / physiopathology
  • Rats
  • Schizophrenia / etiology*
  • Schizophrenia / pathology


  • Neurotoxins
  • Methylazoxymethanol Acetate