Abstract
The effects of lithium on the potentiation of d-amphetamine-induced hyperlocomotion were evaluated in rapid eye movement (REM) sleep deprived rats. Under control conditions, pretreatment with lithium during 7 days did not modify the hyperlocomotion produced by d-amphetamine. REM sleep deprivation induced a pronounced potentiation of the locomotor response to d-amphetamine. In a stress control group this potentiation also occurred, but to a lesser degree than in the REM sleep deprived group. Lithium pretreatment prevented the increased response to d-amphetamine in both REM sleep deprived and stress control animals. The effects of lithium in REM sleep deprived rats are in accordance with reports that lithium is able to prevent the development of dopamine receptor supersensitivity. However, it cannot be excluded that in both REM sleep deprived and stress control groups the increased response to d-amphetamine is related to noradrenergic changes and/or noradrenergic-dopaminergic interactions. REM sleep deprivation seems to be an interesting model to study the underlying mechanisms of manic-depressive illness.