Frintrop Linda, Trinh Stefanie, Seitz Jochen, Kipp Markus
Institute of Anatomy, Rostock University Medical Center, 18057 Rostock, Germany.
Institute of Neuroanatomy, RWTH Aachen University, 52074 Aachen, Germany.
J Clin Med. 2021 Dec 30;11(1):186. doi: 10.3390/jcm11010186.
Eating behavior is controlled by hypothalamic circuits in which agouti-related peptide-expressing neurons when activated in the arcuate nucleus, promote food intake while pro-opiomelanocortin-producing neurons promote satiety. The respective neurotransmitters signal to other parts of the hypothalamus such as the paraventricular nucleus as well as several extra-hypothalamic brain regions to orchestrate eating behavior. This complex process of food intake may be influenced by glia cells, in particular astrocytes and microglia. Recent studies showed that GFAP astrocyte cell density is reduced in the central nervous system of an experimental anorexia nervosa model. Anorexia nervosa is an eating disorder that causes, among the well-known somatic symptoms, brain volume loss which was associated with neuropsychological deficits while the underlying pathophysiology is unknown. In this review article, we summarize the findings of glia cells in anorexia nervosa animal models and try to deduce which role glia cells might play in the pathophysiology of eating disorders, including anorexia nervosa. A better understanding of glia cell function in the regulation of food intake and eating behavior might lead to the identification of new drug targets.
进食行为受下丘脑回路控制，其中表达刺鼠相关肽的神经元在弓状核被激活时会促进食物摄入，而产生促肾上腺皮质激素原的神经元则促进饱腹感。这些神经递质分别向诸如室旁核等下丘脑其他部位以及几个下丘脑外脑区发出信号，以协调进食行为。食物摄入的这一复杂过程可能受神经胶质细胞影响，尤其是星形胶质细胞和小胶质细胞。最近的研究表明，在实验性神经性厌食症模型的中枢神经系统中，胶质纤维酸性蛋白星形胶质细胞密度降低。神经性厌食症是一种进食障碍，在其众所周知的躯体症状中，会导致脑容量减少，这与神经心理缺陷有关，但其潜在的病理生理学尚不清楚。在这篇综述文章中，我们总结了神经性厌食症动物模型中神经胶质细胞的研究结果，并试图推断神经胶质细胞在包括神经性厌食症在内的进食障碍病理生理学中可能发挥的作用。更好地理解神经胶质细胞在食物摄入和进食行为调节中的功能，可能会带来新药物靶点的发现。
