Amygdalohippocampal and Amygdalocortical Projections in the Primate Brain

Abstract

Several lines of evidence have supported the view that the amygdaloid complex plays a major role in the initiation and maintenance of temporal lobe or ‘psychomotor’ seizures. Chronic stereotaxic depth recordings in intractable epileptics, for example, have demonstrated striking correlations between amygdaloid epileptic discharges and the behavioral changes associated with seizures (Wieser, 1983). Electrical stimulation of the amygdaloid complex can also elicit experiences, such as illusions of perception or memory and emotions, such as fear, which are common manifestations of temporal lobe epilepsy (Gloor et al., 1982). Recent experimental models of temporal lobe epilepsy, such as the kindling paradigm (Le Gal La Salle, 1982) and the use of excitatory neurotoxins (Tremblay and Ben-Ari, 1984) have provided additional evidence that the amygdaloid complex and the closely associated hippocampal formation are particularly vulnerable to seizure-producing conditions. In fact, the amygdala and hippocampus are among the most commonly damaged structures in epileptic encephalopathy (Ounsted et al., 1966; Corsellis and Bruton, 1983). Given this context,it would be of obvious importance to determine the extent and organization of the interconnectivity of these two structures as well as their connections with cortical regions which are likely to subserve the perceptual and cognitive functions that are disrupted during seizures. It is only in the last several years, however, that these connections have been systematically studied.