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.

Social defeat, a paradigm of depression in rats that elicits 22-kHz vocalizations, preferentially activates the cholinergic signaling pathway in the periaqueductal gray

“…Conversely, stimulation of the ventral PAG produced submissive behavior (mainly comprised of immobility/freezing behaviors) without emission of USVs [reviewed in 14]. In addition, lesioning the PAG dramatically alters both innate [9] and learned [43] defensive behaviors. Electrical and excitatory amino acid stimulation of the PAG elicits vocalizations in multiple species [28,34,35,42] and, in contrast, lesions there attenuate or abolish these vocalizations and related emotional behaviors [61].…”

A locus and mechanism of action for associative morphine tolerance

“…The amygdala is implicated in the encoding of affective memories [31][32][33] and in the expression of stimulus-reward associations 34,35 . Additionally, neurons in the amygdala change their pattern of firing in response to emotionally significant stimuli 36,37 .…”

Mechanisms of fear extinction

“…219 Altogether this line of research presents convincing evidence for a role of endogenous opioid release at the level of the vlPAG in error correction in Pavlovian fear acquisition and extinction. It remains to be seen how an error signal orchestrated at the level of the vlPAG modulates plasticity occurring elsewhere in the brain, such as the amygdala; and whether this signal specifically modulates conditioned fear responses that require PAG to be expressed, such as freezing, 221 but not those that operate independently of PAG, such as conditioned suppression. 222 Cannabinoids.…”