Amygdala central nucleus lesions: Effect on heart rate conditioning in the rabbit

Kapp, Bruce S.; Frysinger, Robert C.; Gallagher, Michela; Haselton, James R.

doi:10.1016/0031-9384(79)90304-4

Cited by 535 publications

(307 citation statements)

References 41 publications

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“…There is significant support for a role of the CeN in processing Pavlovian stimulus-reward associations (Kapp et al, 1979;Gallagher et al, 1990;Davis, 1992;Parkinson et al, 2000b) and for the B and LA (the BLA complex) in mediating the affective motivational properties of reward-associated cues (Hatfield et al, 1996;Everitt et al, 2000), including cocaine-associated cues (Whitelaw et al, 1996;Meil and See, 1997). The selective induction of ␥ PKC mRNA in the CeN and B of the Paired and Pavlovian groups may index the reactivation of these two associations but additionally may reflect the role of the CeN to influence conditioned somatic, autonomic, and endocrine responses on exposure to the drug cue .…”

Section: Processing the Cs In The Amygdalamentioning

confidence: 97%

Limbic-Cortical-Ventral Striatal Activation during Retrieval of a Discrete Cocaine-Associated Stimulus: A Cellular Imaging Study with γ Protein Kinase C Expression

Thomas

Everitt

2001

J. Neurosci.

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We investigated the neuronal activation associated with reexposure to a discrete cocaine-associated stimulus using in situ hybridization to quantify the expression of the plasticityregulated gene, ␥ protein kinase C (␥ PKC), in the limbiccortical-ventral striatal system. Groups of rats were trained to self-administer cocaine paired with a light stimulus (Paired) or paired with an auditory stimulus but also receiving light presentations yoked to those in the Paired group (Unpaired). Additional groups received noncontingent cocaine-light pairings (Pavlovian) or saline-light pairings (Saline) that were yoked to the Paired group. After acquisition of self-administration by the Paired and Unpaired groups, all groups had a 3 d drug-and training-free period before being reexposed to noncontingent presentations of the light conditioning stimulus during a 5 min test session in the training context. There were four major patterns of results for regional ␥ PKC expression 2 hr later. (1) Changes occurred only in groups in which the light was predictive of cocaine. (2) Increases were seen in the amygdala, but decreases were seen in the medial prefrontal cortex. (3) No changes were seen in the hippocampus. (4) Although changes were observed in the basal and central nuclei of the amygdala and the prelimbic cortex in both the Paired and Pavlovian groups, additional changes were observed in the nucleus accumbens core, lateral amygdala, and anterior cingulate cortex in the Pavlovian group. These results suggest not only that regionally selective alterations in ␥ PKC expression are an index of the retrieval of Pavlovian associations formed between a drug and a discrete stimulus, but also that a distinct neural circuitry may underlie Pavlovian stimulus-reward associations in cocaine-experienced rats.

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Section: Processing the Cs In The Amygdalamentioning

confidence: 97%

Limbic-Cortical-Ventral Striatal Activation during Retrieval of a Discrete Cocaine-Associated Stimulus: A Cellular Imaging Study with γ Protein Kinase C Expression

Thomas

Everitt

2001

J. Neurosci.

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“…A central role of amygdalar neurons is indicated by findings that amygdala lesions impair the acquisition of conditioned immobility (LeDoux et al, 1988; Fanselow and K im, 1994;LeDoux, 1995), autonomic responding (Blanchard and Blanchard, 1972;Spevack et al, 1975;Kapp et al, 1979;Gentile et al, 1986;Iwata et al, 1986;Helmstetter, 1992) and fear-potentiated startle behavior (Davis, 1986(Davis, , 1992Hitchcock and Davis, 1987;Sananes and Davis, 1992). Also, amygdalar neurons exhibit associative, training-induced activity (TIA) during Pavlovian conditioning (Umemoto and Olds, 1975;Applegate et al, 1982;Pascoe and Kapp, 1985;Nishijo et al, 1988; Muramoto et al, 1993;McEchron et al, 1995;Quirk et al, 1995).…”

Section: Abstract: Limbic Thalamus; Cingulate Cortex; Amygdala; Learmentioning

confidence: 99%

Medial Geniculate Lesions Block Amygdalar and Cingulothalamic Learning-Related Neuronal Activity

Poremba

Gabriel

1997

J. Neurosci.

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This study assessed the role of the thalamic medial geniculate (MG) nucleus in discriminative avoidance learning, wherein rabbits acquire a locomotory response to a tone [conditioned stimulus (CS)ϩ] to avoid a foot shock, and they learn to ignore a different tone (CSϪ) not predictive of foot shock. Limbic (anterior and medial dorsal) thalamic, cingulate cortical, or amygdalar lesions severely impair acquisition, and neurons in these areas develop training-induced activity (TIA): more firing to the CSϩ than to the CSϪ. MG neurons exhibit TIA during learning and project to the amygdala. The MG neurons may supply afferents essential for amygdalar and cingulothalamic TIA and for avoidance learning. To test this hypothesis, bilateral electrolytic or excitotoxic ibotenic acid MG nuclear lesions were induced, and multiunit recording electrodes were chronically implanted into the anterior and posterior cingulate cortex, the anterior-ventral and medial-dorsal thalamic nuclei, and the basolateral nucleus of the amygdala before training. Learning was severely impaired and TIA was abolished in all areas in rabbits with lesions. Thus learning and TIA require the integrity of the MG nucleus. Only damage in the medial MG division was significantly correlated with the learning deficit. The lesions abolished the sensory response of amygdalar neurons, and they attenuated (but did not eliminate) the sensory response of cingulothalamic neurons, suggesting the existence of extra geniculate sources of auditory transmission to the cingulothalamic areas. Key words: limbic thalamus; cingulate cortex; amygdala; learning; instrumental conditioning; anterior ventral nucleus; medial dorsal nucleusThere is currently a great interest in the neural circuitry underlying aversively motivated learning (for review, see Davis, 1992;Gabriel, 1993;Lennartz and Weinberger, 1994;LeDoux, 1995;McGaugh et al., 1995;. A central role of amygdalar neurons is indicated by findings that amygdala lesions impair the acquisition of conditioned immobility (LeDoux et al., 1988; Fanselow and K im, 1994;LeDoux, 1995), autonomic responding (Blanchard and Blanchard, 1972;Spevack et al., 1975;Kapp et al., 1979;Gentile et al., 1986;Iwata et al., 1986;Helmstetter, 1992) and fear-potentiated startle behavior (Davis, 1986(Davis, , 1992Hitchcock and Davis, 1987;Sananes and Davis, 1992). Also, amygdalar neurons exhibit associative, training-induced activity (TIA) during Pavlovian conditioning (Umemoto and Olds, 1975;Applegate et al., 1982;Pascoe and Kapp, 1985;Nishijo et al., 1988; Muramoto et al., 1993;McEchron et al., 1995;Quirk et al., 1995).An involvement of the medial geniculate (MG) nucleus in aversively motivated learning is indicated by the observation of TIA in the medial division of the MG nucleus (MGm) (Olds et al., 1972;Gabriel et al., 1975;Gabriel et al., 1976;Ryugo and Weinberger, 1978;Birt and Olds, 1981;Weinberger, 1982;Edeline, 1990;Edeline and Weinberger, 1992;McEchron et al., 1995), and by impaired conditioning in animals with MG lesions (Iwata et al., 198...

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“…Another possible explanation for the discrepancy between the two studies concerns the extent to which the infralimbic nucleus (IL) was destroyed by the lesions. The IL contributes the majority of vmPFC inputs to the central nucleus of the amygdala (Sesack et al, 1989;Hurley et al, 1991), which plays a key role in the expression of behavioral and autonomic indices of conditioned fear (Kapp et al, 1979;LeDoux et al, 1988;Helmstetter, 1992;McCabe et al, 1992;Powell, 1994;Campeau and Davis, 1995;Maren, 1999;Amorapanth et al, 2000). IL also projects to many of the hypothalamic and midbrain sites that mediate fear responses (Sesack et al, 1989;Hurley et al, 1991).…”

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confidence: 99%

The Role of Ventromedial Prefrontal Cortex in the Recovery of Extinguished Fear

et al. 2000

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Conditioned fear responses to a tone paired with footshock extinguish when the tone is presented repeatedly in the absence of shock. Rather than erase the tone-shock association, extinction is thought to involve new learning accompanied by inhibition of conditioned responding. Despite much interest in extinction from a clinical perspective, little is known about the neural circuits that are involved. Although the prefrontal cortex has a well established role in the inhibition of inappropriate behaviors, previous reports have disagreed as to the role of the ventromedial prefrontal cortex (vmPFC) in extinction. We have reexamined the effects of electrolytic vmPFC lesions made before training on the acquisition, extinction, and recovery of conditioned fear responses in a 2 d experiment. On Day 1 vmPFC lesions had no effect on acquisition or extinction of conditioned freezing and suppression of bar pressing. On Day 2 sham rats recovered only 27% of their acquired freezing, whereas vmPFC-lesioned rats recovered 86%, which was indistinguishable from a control group that never received extinction. The high recovery in lesioned rats could not be attributed to decreased motivation or altered sensitivity to footshock. vmPFC lesions that spared the caudal infralimbic (IL) nucleus had no effect. Thus, the vmPFC (particularly the IL nucleus) is not necessary for expression of extinction, but it is necessary for the recall of extinction learning after a long delay. These data suggest a role of the vmPFC in consolidation of extinction learning or the recall of contexts in which extinction took place.Key words: extinction; infralimbic; prelimbic; fear conditioning; amygdala; inhibition Prefrontal cortex has long been implicated in inhibition of inappropriate responses. Lesions of medial prefrontal cortex (mPFC) cause perseverative responding in animals and humans and cause deficits in reversal tasks (for review, see Kolb, 1984;Fuster, 1997). Perseverative responding in prefrontal animals was extended to conditioned fear when it was shown that rats with mPFC lesions could acquire freezing responses to a tone paired with a footshock, but they required many more days to extinguish those responses when the tone was presented alone (Morgan et al., 1993). More recent data support the hypothesis that mPFC is involved in the inhibition of fear responses (Bremner et al., 1999;Herry et al., 1999;Morrow et al., 1999), and it has been suggested that deficits in extinction of conditioned fear may cause certain anxiety disorders (Charney and Deutch, 1996;Pitman, 1997).Many questions remain, however, concerning the role of the ventromedial prefrontal cortex (vmPFC) in extinction of fear. Following the original report by Morgan et al. (1993), Gewirtz et al. (1997 found no effect of vmPFC lesions on extinction of conditioned fear responses. To explain this discrepancy, Gewirtz et al. (1997) suggested that the prolonged extinction might have been attributable to increased acquisition in the lesioned animals, which was masked by asymptotic freezi...

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Amygdala central nucleus lesions: Effect on heart rate conditioning in the rabbit

Cited by 535 publications

References 41 publications

Limbic-Cortical-Ventral Striatal Activation during Retrieval of a Discrete Cocaine-Associated Stimulus: A Cellular Imaging Study with γ Protein Kinase C Expression

Limbic-Cortical-Ventral Striatal Activation during Retrieval of a Discrete Cocaine-Associated Stimulus: A Cellular Imaging Study with γ Protein Kinase C Expression

Medial Geniculate Lesions Block Amygdalar and Cingulothalamic Learning-Related Neuronal Activity

The Role of Ventromedial Prefrontal Cortex in the Recovery of Extinguished Fear

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