Holubiec Mariana I, Romero Juan I, Blanco Eduardo, Tornatore Tamara Logica, Suarez Juan, Rodríguez de Fonseca Fernando, Galeano Pablo, Capani Francisco
Facultad de Medicina, Instituto de Investigaciones Cardiológicas "Prof. Dr. Alberto C. Taquini" (ININCA), Universidad de Buenos Aires (CONICET), Buenos Aires, Argentina.
Instituto de Investigaciones Bioquímicas de Buenos Aires (CONICET), Fundación Instituto Leloir, Buenos Aires, Argentina.
Neurosci Lett. 2017 Jul 13;653:269-275. doi: 10.1016/j.neulet.2017.05.068. Epub 2017 Jun 1.
Endocannabinoids (eCBs) and acylethanolamides (AEs) have lately received more attention due to their neuroprotective functions in neurological disorders. Here we analyze the alterations induced by perinatal asphyxia (PA) in the main metabolic enzymes and receptors of the eCBs/AEs in the dorsal striatum of rats. To induce PA, we used a model developed by Bjelke et al. (1991). Immunohistochemical techniques were carried out to determine the expression of neuronal and glial markers (NeuN and GFAP), eCBs/AEs synthesis and degradation enzymes (DAGLα, NAPE-PLD and FAAH) and their receptors (CB1 and PPARα). We found a decrease in NAPE-PLD and PPARα expression. Since NAPE-PLD and PPARα take part in the production and reception of biochemical actions of AEs, such as oleoylethanolamide, these results may suggest that PA plays a key role in the regulation of this system. These data agree with previous results obtained in the hippocampus and encourage us to develop further studies using AEs as potential neuroprotective compounds.
内源性大麻素（eCBs）和酰基乙醇酰胺（AEs）因其在神经疾病中的神经保护功能，近来受到了更多关注。在此，我们分析围产期窒息（PA）对大鼠背侧纹状体中eCBs/AEs的主要代谢酶和受体所诱导的变化。为诱导PA，我们采用了Bjelke等人（1991年）开发的模型。运用免疫组织化学技术来确定神经元和胶质细胞标志物（NeuN和GFAP）、eCBs/AEs合成与降解酶（DAGLα、NAPE-PLD和FAAH）及其受体（CB1和PPARα）的表达。我们发现NAPE-PLD和PPARα的表达有所下降。由于NAPE-PLD和PPARα参与了AEs（如油酰乙醇胺）生化作用的产生和接收，这些结果可能表明PA在该系统的调节中起关键作用。这些数据与先前在海马体中获得的结果一致，并促使我们开展进一步研究，将AEs用作潜在的神经保护化合物。
