Somnolence, recovery and hyposomnia following ventro-medial diencephalic lesions in the rat

Abstract

1. 1. The disturbances in sleep and wakefulness that follow large posterior hypothalamic and subthalamic lesions were assessed in fourteen rats. 2. 2. The analysis of the time course of the lesion effects showed that disturbances in sleep and wakefulness exhibited a consistent pattern that could be divided into the following four successive stages: (a) Hyperactivity, lasting from 4 to 8 h, and consisting of relentless locomotion with desynchronized EEG activity, commenced immediately after the lesions (made through chronically implanted electrodes). (b) Somnolence, a sleep-like state, lasted from 1 to 4 days. During an initial continuous phase of somnolence there were occasional bursts of muscle activity but the EEG remained synchronized. During the second portion, the interrupted phase of somnolence, there were brief spontaneous arousals accompanied by EEG desynchronization. (c) Recovery from somnolence was gradual, but complete, in every animal which survived more than 8 days, including some animals with lesions that completely destroyed the medial half of the caudal diencephalon. However, a deficit in locomotor activity during wakefulness persisted for months. (d) Hyposomnia, subnormal amounts of sleep, followed recovery from somnolence in most animals. A 10–50% reduction in sleep persisted at least 4 months after the lesions. 3. 3. Active sleep was completely suppressed during the continuous phase of somnolence. This state reappeared, in greatly reduced amounts, at the time when brief arousal was also observed. The proportion of active sleep returned to normal during recovery with a time course similar to the recovery of wakefulness. Rare episodes of neck muscle atonia without accompanying EEG desynchronization were observed only during the continuous phase of somnolence. 4. 4. Analysis of sleep patterns and arousal thresholds after partial recovery from somnolence suggested that the lesions of the diencephalic reticular area released quiet sleep mechanisms and inhibited initiation of wakefulness and active sleep.