Abstract

ObjectivesThe amygdala is known to be a key neural structure in many neuropsychiatric disorders. Primarily known for its involvement in fear regulation, the amygdala also plays a critical role in appetitive flexible decision-making. Yet, its contribution to the development of flexible goal-directed behavior has not been thoroughly examined.DesignThe current study examined flexible decision-making abilities after neonatal amygdala lesions in nonhuman primates using a behavioral paradigm known to measure the flexible monitoring of goal-directed choices in rodents, monkeys, and humans.MethodRhesus monkeys of both sexes were divided into two groups, a sham-operated control group (N=4) and a group with neonatal neurotoxic amygdala lesions (N=5). Animals received the lesions at 1–2 weeks and were tested at both four and six years of age on a concurrent discrimination reinforcer devaluation task.ResultsAlthough neonatal amygdala damage spared learning stimulus-reward associations, it severely impaired the ability to flexibly shift object choices away from those items associated with devalued food rewards. The results were similar to those obtained in monkeys that had acquired the same lesions in adulthood.ConclusionsThus, the amygdala is critical for appetitive decision-making, and provide further evidence of little functional sparing after early amygdala insult. The findings are discussed in relation to other behavioral measures on the same animals and to clinical neuropsychiatric disorders.

Highlights

  • A growing trend in neuropsychiatric research is the transition from relying primarily on behavioral symptom-based diagnoses [1] to include biomarkers as a clinical basis for diagnosis [2,3]

  • Conclusions—the amygdala is critical for appetitive decision-making, and provide further evidence of little functional sparing after early amygdala insult

  • The findings are discussed in relation to other behavioral measures on the same animals and to clinical neuropsychiatric disorders

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Summary

Introduction

A growing trend in neuropsychiatric research is the transition from relying primarily on behavioral symptom-based diagnoses [1] to include biomarkers (endophenotypes) as a clinical basis for diagnosis [2,3]. Amygdala dysfunction has been identified in many neuropsychiatric disorders including classic developmental disorders such as Autism [4], William’s Syndrome [5], and Schizophrenia [6,7], Post-Traumatic Stress Disorder (PTSD) [8], and other anxiety disorders [9]. These syndromes are thought to have a strong developmental component [10]. The present paper will inform on the contribution of the amygdala to the development of flexible regulation of goal-directed behaviors

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