Sleep and other behavioural effects induced by acetylcholinic stimulation of basal temporal cortex and striate structures

Abstract

Summary Hypogenic structures in the temporal lobe and basal ganglia were mapped out by the method of localized chemical stimulation which has recently disclosed a hypnogenic limbic midbrain pathway. Specially devised cannulae and electrodes were permanently implanted in the brain of cats, and a correlated study of the behavioural and electrographic effects was carried out. It was found that the application of minute crystals of acetylcholine successively induced the behavioural and electrographic manifestations of the two patterns of sleep, only when applied to certain anatomical structures including the prepyriform and periamygdaloid cortex, the olfactory tubercle, the anterior and posterior sylvian cortex, the entopeduncular nucleus, the globus pallidus, the putamen, and the caudate nucleus. Chemically induced sleep was readily conditioned to the external environment. In a few experiments, narcoleptic and cataplectic-like responses were elicited from the pyriform cortex. Cortically induced sleep was prevented by lesions involving either the medial forebrain bundle (MFB), or the n. ventralis anterior of the thalamus, or the n. reticularis gigantocellularis in the rostral medullary tegmentum. Lesions involving midbrain or pontine structures, including the n. reticularis pontis caudalis, were ineffective in interfering with acetylcholinic sleep of cortical origin. Anatomical connections between the hypnogenic pyriform cortex and the MFB were confirmed by neuronography. In addition to the sleep effects, a wide variety of autonomic and somatomotor responses, sometimes integrated as emotional behaviour or seizures, were obtained by acetylcholinic stimulation of other anatomical loci. Besides demonstrating cortical hypnogenic areas corresponding to the uncus and insula of the primate brain, the abovementioned results indicate the important participation of the MFB and of the bulbar reticular formation in cortically induced sleep. It is suggested that the clinical syndrome of narcolepsycataplexy may arise from parosysmal activity in the pyriform cortex.