title: Growth hormone biases amygdala network activation after fear learning.
abstract: Prolonged stress exposure is a risk factor for developing posttraumatic stress disorder, a disorder characterized by the 'over-encoding' of a traumatic experience. A potential mechanism by which this occurs is through upregulation of growth hormone (GH) in the amygdala. Here we test the hypotheses that GH promotes the over-encoding of fearful memories by increasing the number of neurons activated during memory encoding and biasing the allocation of neuronal activation, one aspect of the process by which neurons compete to encode memories, to favor neurons that have stronger inputs. Viral overexpression of GH in the amygdala increased the number of amygdala cells activated by fear memory formation. GH-overexpressing cells were especially biased to express the immediate early gene c-Fos after fear conditioning, revealing strong autocrine actions of GH in the amygdala. In addition, we observed dramatically enhanced dendritic spine density in GH-overexpressing neurons. These data elucidate a previously unrecognized autocrine role for GH in the regulation of amygdala neuron function and identify specific mechanisms by which chronic stress, by enhancing GH in the amygdala, may predispose an individual to excessive fear memory formation.
authors.affiliation: McGovern Institute for Brain Research, Department of Brain and Cognitive Sciences, Massachusetts Institute of Technology, Cambridge, MA, USA.
authors.forename: B
authors.initials: B
authors.lastname: Gisabella
authors.affiliation: McGovern Institute for Brain Research, Department of Brain and Cognitive Sciences, Massachusetts Institute of Technology, Cambridge, MA, USA.
authors.forename: S
authors.initials: S
authors.lastname: Farah
authors.affiliation: McGovern Institute for Brain Research, Department of Brain and Cognitive Sciences, Massachusetts Institute of Technology, Cambridge, MA, USA.
authors.forename: X
authors.initials: X
authors.lastname: Peng
authors.affiliation: McGovern Institute for Brain Research, Department of Brain and Cognitive Sciences, Massachusetts Institute of Technology, Cambridge, MA, USA.
authors.forename: A
authors.initials: A
authors.lastname: Burgos-Robles
authors.affiliation: McGovern Institute for Brain Research, Department of Brain and Cognitive Sciences, Massachusetts Institute of Technology, Cambridge, MA, USA.
authors.forename: S H
authors.initials: SH
authors.lastname: Lim
authors.affiliation: McGovern Institute for Brain Research, Department of Brain and Cognitive Sciences, Massachusetts Institute of Technology, Cambridge, MA, USA.
authors.forename: K A
authors.initials: KA
authors.lastname: Goosens
mesh_terms: D000679:Amygdala / Q000502:physiology*; D000818:Animals; D066272:Basolateral Nuclear Complex / Q000502:physiology; D002478:Cells, Cultured; D003214:Conditioning, Classical / Q000502:physiology*; D049229:Dendritic Spines / Q000502:physiology; D005239:Fear / Q000502:physiology*; D013006:Growth Hormone / Q000502:physiology*; D008297:Male; D011939:Mental Recall / Q000502:physiology; D018613:Microscopy, Confocal; D009415:Nerve Net / Q000502:physiology*; D009474:Neurons / Q000502:physiology; D051381:Rats; D020318:Rats, Long-Evans; D011999:Recruitment, Neurophysiological / Q000502:physiology; D012153:Retention, Psychology / Q000502:physiology
chemical_list: D013006:Growth Hormone