Abstract

Lesions in the septal area of the forebrain or in the dorsomedial tegmentum of the brainstem produced a 3-fold prolongation of thiopential-induced sleep. Slices of cerebral neocortex taken from lesioned and control animals were then incubated in vitro, and changes in oxygen consumption after addition of thiopental or potassium chloride were followed manometrically. The rate of glucose-supported respiration of cortical slices was the same for all groups of rats. Na thiopental (125 mM) produced a greater depression of respiration in slices taken from rats with septal or dorsomedial tegmentum lesions (50-52%) than in slices taken from control rats (27-33%). Potassium chloride (100 mM) produced a greater respiratory stimulation in neocortex of control rats (81-108%) than in neocortex of rats with septal or dorsomedial tegmentum lesions (35-36%). In the presence of Na thiopental (0.2 mM) the potassium-stimulated respiration of cortical slices taken from septal or dorsomedial tegmentum-lesioned rats (15-18%) was lower than in slices taken from control rats (43-58%). The changes in neocortex produced by septal and dorsomedial tegmentum lesions (decreased excitability and increased sensitivity to thiopental) were suggested to be responsible for the occurrence of increased thiopental-induced sleep.