Prenatal protein malnutrition decreases KCNJ3 and 2DG activity in rat prefrontal cortex

Neuroscience. 2015 Feb 12:286:79-86. doi: 10.1016/j.neuroscience.2014.11.005. Epub 2014 Nov 18.

Abstract

Prenatal protein malnutrition (PPM) in rats causes enduring changes in brain and behavior including increased cognitive rigidity and decreased inhibitory control. A preliminary gene microarray screen of PPM rat prefrontal cortex (PFC) identified alterations in KCNJ3 (GIRK1/Kir3.1), a gene important for regulating neuronal excitability. Follow-up with polymerase chain reaction and Western blot showed decreased KCNJ3 expression in the PFC, but not hippocampus or brainstem. To verify localization of the effect to the PFC, baseline regional brain activity was assessed with (14)C-2-deoxyglucose. Results showed decreased activation in the PFC but not hippocampus. Together these findings point to the unique vulnerability of the PFC to the nutritional insult during early brain development, with enduring effects in adulthood on KCNJ3 expression and baseline metabolic activity.

Keywords: 2-deoxyglucose; GIRK1; KCNJ3; brain activity; prefrontal cortex; prenatal protein malnutrition.

Publication types

  • Research Support, N.I.H., Extramural

MeSH terms

  • Animals
  • Deoxyglucose / metabolism*
  • Down-Regulation
  • Female
  • G Protein-Coupled Inwardly-Rectifying Potassium Channels / genetics*
  • Gene Expression
  • Male
  • Malnutrition / genetics*
  • Malnutrition / metabolism*
  • Prefrontal Cortex / metabolism*
  • Pregnancy
  • Prenatal Nutritional Physiological Phenomena*
  • Rats
  • Rats, Long-Evans

Substances

  • G Protein-Coupled Inwardly-Rectifying Potassium Channels
  • Kcnj3 protein, rat
  • Deoxyglucose