Gietzen D W, Magrum L J
Department of Anatomy, Physiology and Cell Biology, School of Veterinary Medicine and Food Intake Laboratory, University of California-Davis, Davis, CA 95616, USA.
J Nutr. 2001 Mar;131(3):851S-855S. doi: 10.1093/jn/131.3.851S.
The anterior piriform cortex (APC) of the rat is thought to be the site of indispensable amino acid (IAA) chemosensation in the brain. The branched-chain amino acids, including leucine, are among the IAA that are recognized in the APC. The behavioral outcome of IAA deficiency is an anorectic response. The specific transduction mechanisms by which IAA deficiency and repletion activate the APC are not fully understood, but clearly phosphorylation of proteins, increases in intracellular calcium, and expression of the immediate early gene c-fos, which are among the earliest events occurring after the initial drop in the concentration of the limiting IAA, cause stimulation in the APC. Subsequently, several neurotransmitter systems, including those for norepinephrine, GABA, serotonin, dopamine and nitric oxide, are activated in the APC of rats that have consumed an IAA-imbalanced diet. These systems appear to modulate the output cells from the APC, glutamatergic pyramidal cells that send neural signals to activate subsequent relays in the brain. Ultimately, the feeding circuits of the brain carry out the anorectic response. Continued consumption of a diet containing an IAA imbalance causes a conditioned taste aversion to the diet in all animals that have been studied. Such learning involves synaptic reorganization, requiring both degradation and synthesis of protein, along with alterations in genomic activity.
大鼠的前梨状皮质（APC）被认为是大脑中必需氨基酸（IAA）化学感受的位点。包括亮氨酸在内的支链氨基酸属于在APC中被识别的IAA。IAA缺乏的行为结果是厌食反应。IAA缺乏和补充激活APC的具体转导机制尚未完全了解，但在限制性IAA浓度最初下降后最早发生的事件中，蛋白质磷酸化、细胞内钙增加以及即刻早期基因c-fos的表达会引起APC的刺激。随后，在食用IAA失衡饮食的大鼠的APC中，包括去甲肾上腺素、γ-氨基丁酸（GABA）、5-羟色胺、多巴胺和一氧化氮的几种神经递质系统被激活。这些系统似乎调节来自APC的输出细胞，即谷氨酸能锥体细胞，这些细胞发送神经信号以激活大脑中的后续中继。最终，大脑的进食回路产生厌食反应。持续食用含有IAA失衡的饮食会导致所有已研究动物对该饮食产生条件性味觉厌恶。这种学习涉及突触重组，需要蛋白质的降解和合成以及基因组活性的改变。
