title: Different projections of the central amygdaloid nucleus mediate autonomic and behavioral correlates of conditioned fear.
abstract: The purpose of the present study was to determine whether lesions of areas projected to by the central amygdaloid nucleus (ACE) would disrupt the classical conditioning of autonomic and/or behavioral emotional responses. The areas studied included 3 projection targets of the ACE: the lateral hypothalamic area (LH), midbrain central gray (CG) region, and bed nucleus of the stria terminalis (BNST). Lesions were made either electrolytically or by microinjection of ibotenic acid, which destroys local neurons without interrupting fibers of passage. Two weeks later, the animals were classically conditioned by pairing an acoustic stimulus with footshock. The next day, conditioned changes in autonomic activity (increases in arterial pressure) and emotional behavior ("freezing," or the arrest of somatomotor activity) evoked by the acoustic conditioned stimulus (CS) were measured during extinction trials. Electrolytic and ibotenic acid lesions of the LH interfered with the conditioned arterial pressure response, but did not affect conditioned freezing. Electrolytic lesions of the rostral CG disrupted conditioned freezing but not conditioned changes in arterial pressure. Ibotenic acid injected into the rostral CG reduced neither the arterial pressure nor the freezing response. Injection of ibotenic acid in the caudal CG, like electrolytic lesions of the rostral CG, disrupted the freezing, but not the arterial pressure response. Injection of ibotenic acid into the BNST had no effect on either response. These data demonstrate that neurons in the LH are involved in the autonomic, but not the behavioral, conditioned response pathway, whereas neurons in the caudal CG are involved in the behavioral, but not the autonomic, pathway. Different efferent projections of the central amygdala thus appear to mediate the behavioral and autonomic concomitants of conditioned fear.
authors.affiliation: Division of Neurobiology, Cornell University Medical College, New York, New York 10021.
authors.forename: J E
authors.initials: JE
authors.lastname: LeDoux
authors.forename: J
authors.initials: J
authors.lastname: Iwata
authors.forename: P
authors.initials: P
authors.lastname: Cicchetti
authors.forename: D J
authors.initials: DJ
authors.lastname: Reis
mesh_terms: D000679:Amygdala / Q000502:physiology*; D000818:Animals; D001341:Autonomic Nervous System / Q000502:physiology*; D001522:Behavior, Animal / Q000502:physiology*; D003214:Conditioning, Classical; D005239:Fear / Q000502:physiology*; D007031:Hypothalamus / Q000502:physiology; D008297:Male; D008636:Mesencephalon / Q000502:physiology; D010487:Periaqueductal Gray / Q000502:physiology; D051381:Rats; D011919:Rats, Inbred Strains; D009435:Synaptic Transmission; D013788:Thalamus / Q000502:physiology