title: Collateral sprouting of somatostatin-immunoreactive axons after partial deafferentation of the central nucleus of the rat amygdala.
abstract: These experiments utilize a paradigm developed to study plastic responses of peptidergic neurons in a discrete brain area following deafferentation. The central nucleus of the amygdala (CNA) is richly innervated by somatostatin-immunoreactive (SS-I) terminal axons. In the course of preliminary light microscopic (LM) investigations by this laboratory, changes were observed in the density of presumed SS-I terminals in the rat CNA after lesioning the medial input. The LM finding of increased density of presumed SS-I terminals in the CNA at the 10-day post-lesion stage underscored the need for a quantitative electron microscopic (EM) study of the SS-I components, including an evaluation of synaptic events at different survival periods. At the 3-day post-lesion stage, EM examination showed degenerating axons in the lesioned CNA, many already engulfed by astrocytes. None of the degenerating profiles were SS-I, supporting the view that the lesion did not interrupt, to any significant extent, SS-I axons entering the nucleus. EM surveys of the 10-day post-lesion material demonstrated that degenerated profiles had almost completely disappeared. Numbers of SS-I axon terminals, particularly of smaller-sized profiles, were increased by 22% over control value. Synaptic frequency was decreased by 16% below control value. Numbers of SS-I terminals making synapses were increased 3.4% above control value. At the 30-day post-lesion stage, the total number of SS-I terminal axons had increased 86% over controls, whereas the synaptic frequency had decreased by about a third below controls. The absolute number of SS-I terminals engaging in synapses had increased by 24% over controls. The 90-day post-lesion CNA showed a further increase in the number of SS-I axon profiles: 136% over control value. The synapse-to-axon ratio (synaptic frequency) of 27% was similar to that observed for the CNA from the unlesioned side or from unoperated animals. At this stage the number of SS-I synapses had increased by 135% over controls. This model presents many possibilities for studying neuroplasticity, particularly involving peptidergic neurons of the central autonomic nervous system.
authors.affiliation: Department of Anatomy, College of Medicine, University of Iowa, Iowa City 52242.
authors.forename: T
authors.initials: T
authors.lastname: Gotow
authors.forename: T H
authors.initials: TH
authors.lastname: Williams
authors.forename: J Y
authors.initials: JY
authors.lastname: Jew
authors.forename: M D
authors.initials: MD
authors.lastname: Cassell
authors.forename: M
authors.initials: M
authors.lastname: Palkovits
authors.forename: P H
authors.initials: PH
authors.lastname: Hashimoto
mesh_terms: D000679:Amygdala / Q000502:physiology* / Q000648:ultrastructure; D000818:Animals; D001369:Axons / Q000502:physiology* / Q000648:ultrastructure; D007150:Immunohistochemistry; D008297:Male; D008854:Microscopy, Electron; D009473:Neuronal Plasticity; D051381:Rats; D011919:Rats, Inbred Strains; D013004:Somatostatin / Q000378:metabolism*; D013569:Synapses / Q000502:physiology / Q000648:ultrastructure
chemical_list: D013004:Somatostatin