Danguir J
Nature. 1983;304(5922):163-4. doi: 10.1038/304163a0.
Interest in the Brattleboro diabetes insipidus rat has resurged with the recent increase in research on brain peptides. Various reports have suggested that in these rats, the impaired ability for memory consolidation is due essentially to a chronic lack of vasopressin. On the other hand, sleep stages and particularly the paradoxical phase of sleep have been shown to have a key role in the processes of learning and memory consolidation. Curiously, the possible involvement of sleep deficits in the impairment of memory function in the Brattleboro rat has never been suspected. Here I report a significant reduction (38%) in the daily duration of paradoxical sleep (PS) in the homozygous diabetes insipidus (HODI) rat compared to the heterozygous Long Evans strain. Normal or increased durations of PS were observed after intravenous (i.v.) administration of vasopressin but also when the normal daily water intake (240 ml) was infused i.v. These results provide direct evidence that PS deficits in the HODI rat are not due to the absence of vasopressin. They also suggest that the impaired ability for learning and memory processes are probably due to the impairment of PS rather than to some direct consequence of the hereditary lack of vasopressin.
随着近期对脑肽研究的增加，人们对布拉德福德尿崩症大鼠的兴趣再度兴起。各种报告表明，在这些大鼠中，记忆巩固能力受损主要是由于长期缺乏抗利尿激素。另一方面，睡眠阶段尤其是睡眠的异相阶段已被证明在学习和记忆巩固过程中起关键作用。奇怪的是，从未有人怀疑过睡眠不足可能与布拉德福德大鼠记忆功能受损有关。在此，我报告，与杂合的长 Evans 品系相比，纯合尿崩症（HODI）大鼠的每日异相睡眠（PS）时长显著减少（38%）。静脉注射（i.v.）抗利尿激素后，PS 时长正常或增加，静脉输注正常日饮水量（240 毫升）时也是如此。这些结果提供了直接证据，表明 HODI 大鼠的 PS 不足并非由于缺乏抗利尿激素。它们还表明，学习和记忆过程能力受损可能是由于 PS 受损，而非遗传性抗利尿激素缺乏的某些直接后果。
