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J E LeDoux

Publications and source records attributed to J E LeDoux.

At least 91 records · Page 5Linked to original sources
PubMed1990

The lateral amygdaloid nucleus: sensory interface of the amygdala in fear conditioning.

Previous work has implicated projections from the acoustic thalamus to the amygdala in the classical conditioning of emotional responses to auditory stimuli. The purpose of the present studies was to determine whether the lateral amygdaloid nucleus (AL), which is a major subcortical target of projections from the acoustic thalamus, might be the sensory interface of the amygdala in emotional conditioning. Lesions were placed in AL of rats and the effects on emotional conditioning were examined. Lesions of AL, but not lesions of the striatum above or the cortex adjacent to the AL, interfered with emotional conditioning. Lesions that only partially destroyed AL or lesions placed too ventrally that completely missed AL had no effect. AL lesions did not affect the responses elicited following nonassociative (random) training. AL is thus an essential link in the circuitry through which auditory stimuli are endowed with affective properties and may function as the sensory interface of the amygdala during emotional learning.

Acoustic Stimulation↗
PubMed1990

Synaptic plasticity in fear conditioning circuits: induction of LTP in the lateral nucleus of the amygdala by stimulation of the medial geniculate body.

Electrical stimulation of the medial geniculate body in the anesthetized rat produces an evoked potential in the lateral nucleus of the amygdala. The potential varies in amplitude with stimulus intensity and reaches peak amplitude in 8.5 msec on the average. High-frequency stimulation of the pathway produces long-lasting increases in the amplitude and slope of the potential. These robust and enduring experience-dependent modifications in neural transmission occur in a pathway known to be involved in the formation of emotional memories and may offer a means for examining the cellular mechanisms of emotional learning, as well as a new approach to questions concerning the relevance of long-term potentiation to normal mnemonic processes.

Amygdala↗
PubMed1988

Dissociation of associative and nonassociative concomitants of classical fear conditioning in the freely behaving rat.

An acoustic stimulus previously paired with footshock elicits stereotyped increases in arterial pressure and heart rate and induces freezing behavior in freely behaving rats. Although the arterial pressure and freezing responses differ between groups given paired and random presentations of the tone and shock, the increases in heart rate do not. These observations, if taken at face value, suggest that the arterial pressure and freezing responses reflect associative learning but that the heart rate change is a nonassociative or a pseudoconditioned response. In this article we describe three experiments aimed at determining why the CS elicits similar increases in heart rate in groups given paired and random training. The first study demonstrates that regardless of the pseudoconditioning control procedure used (random, backwards, shock-alone, or naive), the same pattern of results is obtained: the increases in arterial pressure are greater in the paired than in each control group, but the heart rate rises to the same extent in all groups. The second study determined that the context in which the responses are tested (conditioning apparatus vs. novel test chamber) does not affect the general pattern of results obtained. The third study demonstrates that the superficially similar increases in heart rate in conditioned and pseudoconditioned rats are achieved by different physiological mechanisms: coactivation of the sympathetic and parasympathetic nervous systems in conditioned rats and sympathetic excitation alone in pseudoconditioned rats. Thus, the heart is influenced by associative emotional processes, but heart rate is not, under these conditions, a particularly useful index of those influences.

Animals↗
PubMed1988

Different projections of the central amygdaloid nucleus mediate autonomic and behavioral correlates of conditioned fear.

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.

Amygdala↗
PubMed1987

Cardiovascular responses elicited by stimulation of neurons in the central amygdaloid nucleus in awake but not anesthetized rats resemble conditioned emotional responses.

Cardiovascular responses elicited by electrical stimulation of the central amygdaloid nucleus were examined in awake and anesthetized rats. Stimulation through chronically implanted electrodes evoked increases in arterial pressure and heart rate in awake, freely behaving rats. The responses, which were dependent upon the frequency and the intensity of the stimulus, were not consistently related to the presence of evoked amygdaloid afterdischarges or to evoked behavioral reactions. Following induction of anesthesia, stimuli delivered to the same rats through the same fixed electrodes produced decreases in blood pressure and heart rate. Microinjection of L-glutamate into the amygdala of freely behaving rats also elicited increases in arterial pressure and heart rate, indicating that the cardiovascular changes evoked by electrical stimuli are due to excitation of local neurons rather than fibers of passage. The timing and pattern of the response elicited by electrical stimulation of the amygdala in the awake but not the anesthetized rat closely corresponds with that evoked by an acoustic conditioned emotional stimulus.

Action Potentials↗
PubMed1986

Intrinsic neurons in the amygdaloid field projected to by the medial geniculate body mediate emotional responses conditioned to acoustic stimuli.

In previous experiments we implicated projections from the medial geniculate body (MG) to a subcortical field, involving portions of the posterior caudate-putamen and amygdala, in the classical conditioning of emotional responses to acoustic stimuli in the rat. In the present series of experiments we examined whether intrinsic neurons in the subcortical field mediate emotional conditioning and, if so, whether the critical neurons are contained within the amygdala or the caudate-putamen. Rats were prepared with a unilateral electrolytic lesion of the MG. Contralaterally, intrinsic neurons were destroyed in the subcortical field by microinjection of ibotenic acid. This lesion combination leaves one MG and one subcortical field intact but disconnected. Controls received unilateral injection of phosphate buffer vehicle into the subcortical field contralateral to the MG lesion or were unoperated. After two weeks the animals were instrumented for continuous, computer-assisted recording of arterial pressure and heart rate and subjected to classical conditioning trials involving the presentation of a pure tone in association with foot-shock. The occurrence of the shock with respect to the tone was random for a pseudoconditioned control group. Conditioned changes in mean arterial pressure, heart rate and emotional behavior ('freezing') elicited by the tone were assessed during extinction trials. Following completion of the experiments, the rats were sacrificed and their brains were removed and sectioned using standard procedures. Lesion location and size was evaluated with the assistance of a computer-based image processing system. In unoperated conditioned rats the acoustic stimulus elicited increases in arterial pressure and heart rate, and induced freezing. The arterial pressure and freezing responses differed in conditioned and pseudoconditioned rats, but the heart rate response did not. Therefore, only the arterial pressure and freezing responses reflect the formation of an association between the tone and shock. Destruction of intrinsic neurons in the subcortical field contralateral to a unilateral MG lesion disrupted the associative conditioning of the arterial pressure and freezing responses. These were reduced in magnitude to the level observed in pseudoconditioned rats. The non-associative heart rate change was not affected by the lesions. That ibotenic acid destroyed intrinsic neurons and spared fibers in the subcortical field was demonstrated anatomically and biochemically.(ABSTRACT TRUNCATED AT 400 WORDS)

Amygdala↗
PubMed1986

Disruption of auditory but not visual learning by destruction of intrinsic neurons in the rat medial geniculate body.

The contribution of intrinsic neurons in the medial geniculate body (MG) of the rat to the classical conditioning of emotional responses to acoustic stimuli was examined. Injection of ibotenic acid, which destroys cell bodies but not axons of passage, into the MG disrupted the conditioned changes in mean arterial pressure and emotional behavior elicited by a tone previously associated with footshock. Unconditioned responses elicited by the tone and by the footshock were unaffected. Moreover, the same animals readily learned to associate a visual stimulus with footshock. Thus, destruction of intrinsic neurons in the MG selectively disrupts the conditioning of emotional responses to acoustic stimuli. The MG appears to be the afferent link in a modality specific emotional learning pathway.

Acoustic Stimulation↗
PubMed1986

Destruction of intrinsic neurons in the lateral hypothalamus disrupts the classical conditioning of autonomic but not behavioral emotional responses in the rat.

The present study examined whether destruction of intrinsic neurons in the lateral hypothalamus of the rat would disrupt the acquisition of classically conditioned changes in arterial pressure. Ibotenic acid, a cellular toxin which spares axons of passage, was injected bilaterally in the hypothalamus either medial or lateral to the fornix. After 2 weeks the animals were subjected to classical fear conditioning trials involving the presentation of a tone in association with footshock. The next day changes in arterial pressure and emotional behavior elicited by the tone alone were measured. Destruction of intrinsic neurons in the lateral hypothalamus prevented the normal establishment of the arterial pressure conditioned response but did not affect the behavioral response. Unconditioned arterial pressure responses elicited by the tone and shock were not affected. Medial hypothalamic injections had no effect on any of the responses. The location of the lateral hypothalamic cell loss overlapped with the neurons projecting to the autonomic region of the spinal cord. Intrinsic neurons in the lateral hypothalamus therefore appear to be specifically involved in mediating learned cardiovascular adjustments.

Animals↗
PubMed1986

Interruption of projections from the medial geniculate body to an archi-neostriatal field disrupts the classical conditioning of emotional responses to acoustic stimuli.

We have previously found that the coupling of changes in autonomic activity and emotional behavior to acoustic stimuli through classical fear conditioning survives bilateral ablation of auditory cortex but is disrupted by bilateral lesions of the medial geniculate nucleus or inferior colliculus in rats. Auditory fear conditioning thus appears to be mediated by the relay of acoustic input from the medial geniculate nucleus to subcortical rather than cortical targets. Since the medial geniculate nucleus projects, in addition to auditory cortex, to a striatal field, involving portions of the posterior neostriatum and underlying archistriatum (amygdala), we have sought to determine whether interruption of connections linking the medial geniculate nucleus to this subcortical field also disrupts conditioning. The conditioned emotional response model studied included the measurement of increases in mean arterial pressure and heart rate and the suppression of exploratory activity and drinking by the acoustic conditioned stimulus following delayed classical conditioning, where the footshock unconditioned stimulus appeared at the end of the conditioned stimulus. The peak increase in arterial pressure and the duration of activity and drinking suppression were greater in unoperated animals subjected to delayed conditioning than in pseudoconditioned controls, where the footshock was randomly rather than systematically related to the acoustic stimulus. Increases in heart rate, however, did not differ in conditioned and pseudoconditioned groups. While the arterial pressure and behavioral responses therefore reflect associative conditioning, the heart rate response does not. Rats were prepared with bilateral lesions of the medial geniculate nucleus, bilateral lesions of the striatal field or asymmetrical unilateral lesions destroying the medial geniculate nucleus on one side and the striatal field on the contralateral side. The latter preparation leaves one medial geniculate nucleus and one striatal field intact but disconnected and thus produces a selective auditory deafferentation of the intact striatal field. Control groups included animals with unilateral lesion of the medial geniculate nucleus, with unilateral lesion of the medial geniculate nucleus combined with lesion of the ipsilateral striatal field, unilateral lesion of the medial geniculate combined with lesion of the contralateral anterior neostriatum (a striatal area outside of the medial geniculate nucleus projection field).(ABSTRACT TRUNCATED AT 400 WORDS)

Acoustic Stimulation↗
PubMed1985

Projections to the subcortical forebrain from anatomically defined regions of the medial geniculate body in the rat.

Although the auditory cortex is believed to be the principal efferent target of the medial geniculate body (MG), our recent behavioral studies indicate that in rats the conditioned coupling of emotional responses to an acoustic stimulus is mediated by subcortical projections of the MG. In the present study we have therefore used WGA-HRP as an anterograde and retrograde axonal marker to (1) define the full range of subcortical efferent projections of the MG; (2) identify the cells of origin within the MG of each projection; and (3) determine whether the subregions of the MG that project to subcortical areas receive inputs from acoustic relay nuclei of the mid-brain, particularly the inferior colliculus. The rat MG was first parcelled into three major cytoarchitectural areas: the ventral, medial, and dorsal divisions. The suprageniculate nucleus, located within the body of the MG just dorsal to the medial division, was also identified. Efferent projections of the MG were determined by combined anterograde and retrograde tracing methods. Injections of WGA-HRP in the MG produced anterograde transport to cortex and several subcortical areas, including the posterior caudate-putamen and amygdala, the ventromedial nucleus of the hypothalamus, and the subparafascicular thalamic nucleus. The cells of origin of the subcortical projections were then mapped retrogradely after injections in the anterogradely labeled areas. Injections in the caudate-putamen or amygdala retrogradely labeled the medial division of the MG and the suprageniculate nucleus, as well as several adjacent areas of the posterior thalamus surrounding the MG. In contrast, injections in the ventromedial nucleus of the hypothalamus or the subparafascicular thalamic nucleus only produced labeling in the areas surrounding MG. Afferents to MG from the inferior colliculus were then identified. The central nucleus of the inferior colliculus, the main lemniscal acoustic relay nucleus in the midbrain, was found to project to the ventral and medial divisions of the MG. In contrast, the dorsal cortex and external nucleus of the inferior colliculus project to each division of the MG and to several additional nuclei in adjacent areas of the posterior thalamus. These data demonstrate that the medial division of MG, the suprageniculate nucleus, and immediately adjacent areas of the posterior thalamus provide a direct linkage between auditory neurons in the inferior colliculus and subcortical areas of the forebrain and thereby support the view that thalamic sensory nuclei relay afferent signals to subcortical as well as cortical areas.

Amygdala↗
PubMed1984

Strain difference in fear between spontaneously hypertensive and normotensive rats is mediated by adrenal cortical hormones.

In the present study we sought to determine whether the strain difference in fear reactivity between spontaneously hypertensive rats (SHR) and strain-matched WKY controls might be related to adrenocortical function. SHR and WKY were subjected to adrenalectomy prior to classical fear conditioning. Adrenal cortical steroids were replaced in some animals. Adrenalectomy produced comparable effects on conditioned fear reactivity in SHR and WKY and steroid replacement reversed the effects of adrenalectomy in both strains. However, a larger dose was required to compensate for adrenalectomy in SHR. These date implicate functions related, directly or indirectly, to the adrenal cortex, in the maintenance of the strain difference in fear reactivity.

Adrenal Cortex Hormones↗
PubMed1984

Subcortical efferent projections of the medial geniculate nucleus mediate emotional responses conditioned to acoustic stimuli.

The purpose of this study was to identify the afferent link in the neural pathway which mediates emotional responses coupled to auditory stimuli. We evaluated whether autonomic and behavioral responses elicited by acoustic conditioned emotional stimuli are based on afferent information derived from the auditory cortex or from the auditory thalamic relay station, the medial geniculate nucleus (MG), in rats. The rat auditory cortex was defined through anterograde neuroanatomical tracing studies involving the injection of HRP into MG. Lesions were then placed in the auditory cortex or in MG. After 10 to 20 days the rats were subjected to classical fear conditioning trials involving the pairing of a pure tone with electric footshock. Changes in mean arterial pressure and heart rate and the duration of immobilization ("freezing") and drink suppression elicited by presentation during extinction trials (no footshock) of the acoustic conditioned emotional stimulus were measured. Auditory cortex lesions did not affect the magnitude of the mean arterial pressure or heart rate conditioned responses nor the duration of freezing or drink suppression. In contrast, lesions of MG suppressed the magnitude of both the autonomic and somatomotor (behavioral) conditioned emotional responses but did not affect either autonomic or somatic responses elicited by the footshock unconditioned stimulus. Lesions of the inferior colliculus, the primary source of afferent input to MG, replicated the effects of MG lesions. These findings demonstrate that lesions of MG and lower auditory centers, but not lesions of the auditory cortex, block autonomic and behavioral conditioned emotional responses coupled to acoustic stimuli and indicate that subcortical rather than cortical efferents of MG sustain these responses. Our concurrent observation that MG projects to several subcortical areas (central and lateral amygdala; caudate-putamen; ventromedial hypothalamus) involved in emotional behavior and autonomic function suggests hypotheses concerning subsequent links in this emotional processing pathway.

Acoustic Stimulation↗
PubMed1983

Local cerebral blood flow increases during auditory and emotional processing in the conscious rat.

Local cerebral blood flow was measured in rats by the 14C-labeled iodoantipyrine technique with quantitative autoradiography during the processing of environmental stimuli. Presentation of a tone increased blood flow in the auditory but not the visual pathway. When the animal had previously been conditioned to fear the tone, blood flow additionally increased in the hypothalamus and amygdala. Local cerebral blood flow can thus be used to detect patterns of cerebral excitation associated with transient (30- to 40-second) mental events in experimental animals.

Acoustic Stimulation↗
PubMed1982

Neuroevolutionary mechanisms of cerebral asymmetry in man.

Cerebral asymmetry in man has by and large been interpreted in terms of differences at the level of hemispheric organization. The inadequacy of a hemispheric interpretation as a biological account of asymmetry is discussed and a model of the neural mechanisms of cerebral asymmetry is developed. The model focuses on the functional organization of the inferior parietal cortex in human and non-human primates and accounts for the evolution and expression of cerebral asymmetry in man in terms of specific adaptations in select neural systems of ancestral primate brains.

Animals↗
PubMed1980

Left hemisphere visual processes in a case of right hemisphere symptomatology. Implications for theories of cerebral lateralization.

A patient with a visuospatial disturbance characteristic of posterior right hemisphere disease was examined under different conditions of stimulus presentation. The visuospatial defect, which was shown by the failure to perceive abnormalities concerning the left side of objects and the misperception of spatial relations, was present under conditions of unrestricted visual exposure. However, when the stimulus material was briefly exposed in the right visual field, performance improved substantially. These data suggest that the visuospatial defect seen after right hemisphere disease is atributable to factors other than the incapacity of the left hemisphere to process visuospatial information. Our observations, together with other evidence, lead us to question those theories of cerebral lateralization based on the notion that visuospatial processing is special to the right hemisphere.

Brain Neoplasms↗