Schönheit B
J Hirnforsch. 1982;23(6):681-92.
The influence of early postnatal undernutrition on growth and maturation processes in pyramidal and stellate neurons of the cingulate cortex was investigated quantitatively in Golgi-Kopsch impregnated sections of the rat brain from 11, 20, 35 and 60 days old control and experimental animals. The starvation experiment was performed by separation the offspring from their mother for hours daily during the first three weeks of postnatal life, continued up to the 60th day by feeding only 5 g pellets per day (which a normal demand of about 20 to 25 gram a day). Data of dendritic ramification, length and spine density were collected as parameters for neuronal development and maturation. In undernourished animals a retardation of the neuron maturation was found. The inhibiting effect of starvation was most pronounced during those periods of brain development showing the highest intensity of the maturation processes in controls: these periods are for lamina V pyramids the early postnatal phase, for Lamina III pyramids the early and late postnatal phase, for interneurons the late postnatal phase only. Thus, the pattern of damage reflects the heterochronicity of maturation of different neuron types. The lamina V pyramids with relative rapid postnatal development were less affected, however, their main spine maturation period covering the 11th upto the 20th day in controls was found to be postponed and the spine density reached finally was diminished. The lamina III pyramids were stronger affected by starvation due to their immature state in the beginning of the experiment and their prolonged maturation. These cells showed remarkable deficits in the spine maturation along the apical side and basal dendrites during the first 3 weeks of postnatal life, in the apical main dendrite up to the 60th day. The most striking effect of starvation occurred in interneurons which differentiate postnatally late and slowly. In controls more than 50 per cent of the dendritic spines appear later than on postnatal day 20. In experimentals the spine density was reduced by 40% already on day 20. Moreover, the deficit increased on day 60 to reach a level of about 60%. These results give evidence for a longlasting injury of the neuropil as morphological basis for mental dysfunction.
在11日龄、20日龄、35日龄和60日龄的对照和实验大鼠的大脑戈尔吉-科普希(Golgi-Kopsch)染色切片中,定量研究了出生后早期营养不良对扣带回皮质锥体细胞和星状神经元生长及成熟过程的影响。饥饿实验通过在出生后的前三周每天将幼崽与母亲分离数小时来进行,持续到60日龄,在此期间每天仅喂食5克颗粒饲料(正常需求量约为每天20至25克)。收集树突分支、长度和棘密度的数据作为神经元发育和成熟的参数。在营养不良的动物中发现神经元成熟延迟。饥饿的抑制作用在大脑发育的那些时期最为明显,这些时期在对照中显示出最高强度的成熟过程:对于第V层锥体神经元是出生后早期阶段,对于第III层锥体神经元是出生后早期和晚期阶段,对于中间神经元仅是出生后晚期阶段。因此,损伤模式反映了不同神经元类型成熟的异时性。出生后发育相对较快的第V层锥体神经元受影响较小,然而,它们在对照中覆盖第11天至第20天的主要棘成熟阶段被推迟,最终达到的棘密度降低。第III层锥体神经元在实验开始时处于未成熟状态且成熟过程延长,因此受饥饿影响更大。这些细胞在出生后第一周的前3周,在顶侧和基底树突的棘成熟方面表现出明显缺陷,在顶主树突中直到60日龄都有缺陷。饥饿对出生后分化较晚且较慢的中间神经元产生的影响最为显著。在对照中,超过50%的树突棘在出生后第20天之后出现。在实验动物中,棘密度在第20天就已经降低了40%。此外,在第60天缺陷增加,达到约60%的水平。这些结果为神经毡的长期损伤提供了证据,这是精神功能障碍的形态学基础。