Bernardis L L, Bellinger L L
Neurovisceral-Neuroendocrine Laboratory, Department of Veterans Affairs Medical Center, Buffalo, NY.
Neurosci Biobehav Rev. 1993 Summer;17(2):141-93. doi: 10.1016/s0149-7634(05)80149-6.
This article reviews findings that have accumulated since the original description of the syndrome that follows destruction of the lateral hypothalamic area (LHA). These data comprise the areas of neuroanatomy, body weight regulation, neuroendocrinology, neurochemistry, and intermediary metabolism. Neurons in the LHA are the largest in the hypothalamus, and are topographically well organized. The LHA belongs to the parasympathetic area of the hypothalamus, and connects with all major parts of the brain and the major hypothalamic nuclei. Rats with LHA lesions regulate their body weight set point in a primary manner and not because of destruction of a "feeding center". The lower body weight is not due to finickiness. In the early stages of the syndrome, catabolism and running activity are enhanced, and so is the activity of the sympathetic nervous system (SNS) as shown by increased norepinephrine excretion that normalizes one mo later. The LHA plays a role in the feedback control of body weight regulation different from ventromedial (VMN) and dorsomedial (DMN). Tissue preparations from the LHA promote glucose utilization and insulin release. Although it does not belong to the classical hypothysiotropic area of the hypothalamus, the LHA does affect neuroendocrine secretions. No plasma data on growth hormone are available following electrolytic lesions LHA but electrical stimulation fails to elicit GH secretion. Nevertheless, antiserum raised against the 1-37 fragment of human GHRF stains numerous perikarya in the dorsolateral LHA. The plasma circadian corticosterone rhythm is disrupted in LHA lesioned rats, but this is unlikely due to destruction of intrinsic oscillators. Stimulation studies show a profound role of the LHA in glucose metabolism (glycolysis, glycogenesis, gluconeogenesis), this mechanism being cholinergic. Its role in lipolysis appears not to be critical. In general, stimulation of the VMN elicits opposite effects. Lesion studies in rats show altered in vitro glucose carbon incorporation into several tissue fractions both a few days, and one mo after lesion production. Several of these changes may be due to the reduced food intake, others appear to be due to a "true" lesion effect.
本文回顾了自最初描述下丘脑外侧区（LHA）破坏后所引发综合征以来积累的研究结果。这些数据涵盖神经解剖学、体重调节、神经内分泌学、神经化学和中间代谢等领域。LHA中的神经元是下丘脑中最大的，且在拓扑结构上组织良好。LHA属于下丘脑的副交感神经区域，并与大脑的所有主要部分以及主要的下丘脑核团相连。患有LHA损伤的大鼠主要通过自身调节体重设定点，而非因为“进食中枢”被破坏。体重降低并非由于挑食。在该综合征的早期阶段，分解代谢和奔跑活动增强，交感神经系统（SNS）的活动也增强，这表现为去甲肾上腺素排泄增加，一个月后恢复正常。LHA在体重调节的反馈控制中所起的作用不同于腹内侧（VMN）和背内侧（DMN）。来自LHA的组织制剂可促进葡萄糖利用和胰岛素释放。尽管LHA不属于下丘脑的经典促垂体区，但它确实会影响神经内分泌分泌。在LHA进行电解损伤后，没有关于生长激素的血浆数据，但电刺激未能引发生长激素分泌。然而，针对人GHRF的1 - 37片段产生的抗血清可使背外侧LHA中的许多核周体染色。LHA损伤的大鼠血浆中皮质酮的昼夜节律被打乱，但这不太可能是由于内在振荡器被破坏所致。刺激研究表明LHA在葡萄糖代谢（糖酵解、糖原生成、糖异生）中起重要作用，该机制是胆碱能的。其在脂肪分解中的作用似乎并不关键。一般来说，刺激VMN会引发相反的效果。对大鼠的损伤研究表明，在损伤产生后的几天以及一个月后，体外葡萄糖碳掺入几种组织成分的情况发生了改变。其中一些变化可能是由于食物摄入量减少，其他变化似乎是由于“真正的”损伤效应。
