title: Prefrontal cortical inputs to the basal amygdala undergo pruning during late adolescence in the rat.
abstract: Transformations in affective and social behaviors, many of which involve amygdalar circuits, are hallmarks of adolescence in many mammalian species. In this study, using the rat as a model, we provide the first evidence that afferents of the basal amygdala (BA) undergo significant structural remodeling during adolescence. We used quantitative tract-tracing and gene expression profiling methods to characterize changes in the medial prefrontal cortical (mPFC) inputs to the BA across ages analogous to the late juvenile period [postnatal day (P) 25], late adolescence (P45), and adulthood (P90) in the rat. As assessed after deposition of Fluorogold into the BA, the number of BA-projecting neurons in the mPFC remained stable between P25 and P45 but decreased by about 50% between P45 and P90. Anterograde tract tracing with biotin dextran amine deposits centered in the ventral prelimbic cortex revealed that, during this period, the density of mPFC-derived axon terminals in the BA also decrease significantly, an effect particularly evident in the dorsal basolateral nucleus. Within the BA, there were also highly significant changes in gene expression indicative of neurite or synaptic plasticity, most notably in the Ras/GTPase superfamily, and in pathways that regulate cytoskeletal dynamics and steroid synthesis/lipid metabolism. These data provide convergent evidence that mPFC inputs to the BA are pruned during late adolescence or early adulthood. Moreover, the structural remodeling within these afferents may be accompanied by significant changes in neurite plasticity within the BA.
authors.affiliation: Department of Psychiatry, College of Physicians and Surgeons, Columbia University, New York, New York 10032, USA.
authors.forename: Victoria L
authors.initials: VL
authors.lastname: Cressman
authors.forename: Jordan
authors.initials: J
authors.lastname: Balaban
authors.forename: Sara
authors.initials: S
authors.lastname: Steinfeld
authors.forename: Alexei
authors.initials: A
authors.lastname: Shemyakin
authors.forename: Peter
authors.initials: P
authors.lastname: Graham
authors.forename: Nelly
authors.initials: N
authors.lastname: Parisot
authors.forename: Holly
authors.initials: H
authors.lastname: Moore
mesh_terms: D000375:Aging; D000679:Amygdala / Q000166:cytology / Q000254:growth & development* / Q000502:physiology*; D000818:Animals; D001369:Axons / Q000502:physiology; D001710:Biotin / Q000031:analogs & derivatives; D002452:Cell Count; D003911:Dextrans; D018507:Gene Expression Regulation, Developmental; D008297:Male; D009434:Neural Pathways / Q000166:cytology / Q000254:growth & development / Q000502:physiology; D016501:Neurites / Q000502:physiology; D056325:Neuronal Tract-Tracers; D009474:Neurons / Q000166:cytology / Q000502:physiology*; D010784:Photomicrography; D017397:Prefrontal Cortex / Q000166:cytology / Q000254:growth & development* / Q000502:physiology*; D011897:Random Allocation; D051381:Rats; D017208:Rats, Wistar
chemical_list: D003911:Dextrans; D056325:Neuronal Tract-Tracers; C076397:biotinylated dextran amine; D001710:Biotin