title: Selective lesion of the hippocampus increases the differentiation of immature neurons in the monkey amygdala.
abstract: 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.
authors.affiliation: Laboratory of Brain and Cognitive Development, Department of Medicine, University of Fribourg, 1700 Fribourg, Switzerland.
authors.forename: Loïc J
authors.identifier: 0000-0003-2043-3711
authors.initials: LJ
authors.lastname: Chareyron
authors.affiliation: Department of Psychiatry and Behavioral Sciences, MIND Institute, University of California, Davis, CA 95616.|California National Primate Research Center, University of California, Davis, CA 95616.
authors.forename: David G
authors.initials: DG
authors.lastname: Amaral
authors.affiliation: Laboratory of Brain and Cognitive Development, Department of Medicine, University of Fribourg, 1700 Fribourg, Switzerland; pierre.lavenex@unil.ch.|Laboratory for Experimental Research on Behavior, Institute of Psychology, University of Lausanne, 1015 Lausanne, Switzerland.
authors.forename: Pierre
authors.identifier: 0000-0002-9278-1312
authors.initials: P
authors.lastname: Lavenex
mesh_terms: D000679:Amygdala / Q000473:pathology* / Q000503:physiopathology; D000818:Animals; D000831:Animals, Newborn; D002452:Cell Count; D002454:Cell Differentiation; D002465:Cell Movement; D005260:Female; D006624:Hippocampus / Q000293:injuries* / Q000473:pathology* / Q000503:physiopathology; D008253:Macaca mulatta; D008297:Male; D058953:Neural Stem Cells / Q000473:pathology* / Q000502:physiology; D009473:Neuronal Plasticity; D009474:Neurons / Q000473:pathology / Q000502:physiology
keywords: immature neuron; migration; neurodevelopmental disorders; plasticity; subventricular zone