Sleep deficits in rats with hereditary diabetes insipidus.
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.[1]References
- Sleep deficits in rats with hereditary diabetes insipidus. Danguir, J. Nature (1983) [Pubmed]
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