期刊名称：Proceedings of the National Academy of Sciences
印刷版ISSN：0027-8424
电子版ISSN：1091-6490
出版年度：2016
卷号：113
期号：50
页码：14420-14425
DOI：10.1073/pnas.1604288113
语种：English
出版社：The National Academy of Sciences of the United States of America
摘要：SignificanceA large population of immature neurons has been reported in the ventromedial portion of the adult primate amygdala. Here, we show that selective hippocampal lesions lead to an increase in mature neuron numbers in the monkey amygdala. After adult lesions, the differentiation of immature neurons was essentially restricted to the paralaminar nucleus and was associated with a decrease in the population of immature neurons in the paralaminar nucleus. In contrast, after neonatal lesions, the differentiation of immature neurons involved the paralaminar, lateral, and basal nuclei, and was associated with an increase in the population of immature neurons in the paralaminar nucleus. This is unique evidence of lesion-induced alterations in the number of neurons in the nonhuman primate amygdala. A large population of immature neurons is present in the ventromedial portion of the adult primate amygdala, a region that receives substantial direct projections from the hippocampal formation. Here, we show the effects of neonatal (n = 8) and adult (n = 6) hippocampal lesions on the populations of mature and immature neurons in the paralaminar, lateral, and basal nuclei of the adult monkey amygdala. Compared with unoperated controls (n = 7), the number of mature neurons was about 70% higher in the paralaminar nucleus of neonate- and adult-lesioned monkeys, and 40% higher in the lateral and basal nuclei of neonate-lesioned monkeys. The number of immature neurons in the paralaminar nucleus was 40% higher in neonate-lesioned monkeys and 30% lower in adult-lesioned monkeys. Similar changes in neuron numbers were also found in two monkeys with nonexperimental, selective, bilateral hippocampal damage. These changes in neuron numbers following hippocampal lesions appear to reflect the differentiation of immature neurons present in the paralaminar nucleus. After adult lesions, the differentiation of immature neurons was essentially restricted to the paralaminar nucleus and was associated with a decrease in the population of immature neurons. In contrast, after neonatal lesions, the differentiation of immature neurons involved the paralaminar, lateral, and basal nuclei. It was associated with an increase in the population of immature neurons in the paralaminar nucleus. Such lesion-induced neuronal plasticity sheds new light on potential mechanisms that may facilitate functional recovery following focal brain injury.
