Jonson K M, Lyle J G, Edwards M J, Penny R H
Brain Res Bull. 1976 Jan-Feb;1(1):133-50. doi: 10.1016/0361-9230(76)90056-3.
Exposure of pregnant guinea pigs to an environmental temperature of 42 degrees C for 1 hr daily on Days 20-24 of gestation resulted in a significant reduction in the birthweight and brainweight of newborn offspring. These deficits persisted to early maturity and were still evident at 250 days of age following behavioral testing. Although some degree of postnatal neurogenesis and brain growth had occurred, this was not sufficient to compensate for the retarding influence of prenatal hyperthermia. Heat stress was also observed to seriously impair learning performance on the original discrimination task and this tendency persisted over the subsequent 4 reversals for both initial and perseverative errors. Impaired learning performance was related to reduction in brainweight. Animals with lower brainweights made significantly more initial, perseverative and total number of errors over the 5 problems. In addition, 12 of the 14 behaviorally tested stressed progeny had brainweights that were at least 2 standard deviations below the mean of the controls and as a result were classified as micrencephalic. Although heat stressed animals showed a significant reduction in the number of amacrine synapses in the inner plexiform layer of the retina, performance differences were not atrributed to changes in synaptic organisation of the retinal circuitry or to visual or other ophthalmic defects, but brain function. Animals with higher mean maternal poststressing core temperatures gave birth to progeny which had smaller whole and part wet-brainweights. Examination of the effect of poststressing core temperature on brainweight revealed that brain growth, independent of bodyweight, was retarded when this temperature elevated above 41.5 degrees C. This represented a rise of approximately 2.1 degrees C above normal and for each 1 degree C rise above this temperature, brainweight was reduced by 0.4227 g of the control value. Analysis of the atmospheric content of the incubator during stressing sessions ruled out the possibility that changes in level of oxygen and carbon dioxide may have contributed to the retarding influence on fetal development and learning ability in the guinea pig.
在妊娠期第20 - 24天,将怀孕的豚鼠每天暴露于42摄氏度的环境温度下1小时,导致新生后代的出生体重和脑重显著降低。这些缺陷持续到早期成熟阶段,在行为测试后的250日龄时仍然明显。尽管出生后发生了一定程度的神经发生和脑生长,但这不足以补偿产前高温的抑制作用。还观察到热应激严重损害了最初辨别任务的学习表现,并且这种趋势在随后的4次逆转中对于初始错误和持续性错误均持续存在。学习表现受损与脑重降低有关。脑重较低的动物在5个问题上的初始错误、持续性错误和总错误数量明显更多。此外,在14只接受行为测试的应激后代中,有12只的脑重至少比对照组平均值低2个标准差,因此被归类为小脑症。尽管热应激动物视网膜内网状层无长突细胞突触数量显著减少,但表现差异并非归因于视网膜神经回路的突触组织变化或视觉或其他眼科缺陷,而是脑功能。平均母体应激后核心体温较高的动物所生后代的全脑和部分湿脑重量较小。检查应激后核心体温对脑重的影响发现,当该温度升高至41.5摄氏度以上时,独立于体重的脑生长受到抑制。这比正常温度升高了约2.1摄氏度,并且在此温度以上每升高1摄氏度,脑重就比对照值减少0.4227克。在应激期间对培养箱内大气成分的分析排除了氧气和二氧化碳水平变化可能对豚鼠胎儿发育和学习能力产生抑制影响的可能性。