产前蛋白质营养不良会降低大鼠前额叶皮层中KCNJ3和2-脱氧葡萄糖的活性。
Prenatal protein malnutrition decreases KCNJ3 and 2DG activity in rat prefrontal cortex.
作者信息
Amaral A C, Jakovcevski M, McGaughy J A, Calderwood S K, Mokler D J, Rushmore R J, Galler J R, Akbarian S A, Rosene D L
机构信息
Department of Anatomy & Neurobiology, Boston University School of Medicine, Boston, MA 02118, United States.
Max Planck Institute of Psychiatry, Munich, Germany.
出版信息
Neuroscience. 2015 Feb 12;286:79-86. doi: 10.1016/j.neuroscience.2014.11.005. Epub 2014 Nov 18.
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.
大鼠孕期蛋白质营养不良（PPM）会导致大脑和行为的持久变化，包括认知僵化加剧和抑制控制能力下降。对PPM大鼠前额叶皮质（PFC）进行的初步基因微阵列筛查发现，KCNJ3（GIRK1/Kir3.1）发生了改变，该基因对调节神经元兴奋性很重要。聚合酶链反应和蛋白质印迹法的后续研究表明，PFC中KCNJ3表达降低，但海马体或脑干中未出现这种情况。为了验证这种影响在PFC中的定位，用（14）C-2-脱氧葡萄糖评估了基线区域脑活动。结果显示PFC激活减少，但海马体未出现这种情况。这些发现共同表明，在大脑早期发育过程中，PFC对营养损伤具有独特的易损性，在成年期对KCNJ3表达和基线代谢活动具有持久影响。
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