Growth hormone biases amygdala network activation after fear learning
Name
Gisabella-2016-Growth hormone biases amygdala.pdf
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1.57 MB
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Checksum (MD5)
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Author(s)
Gisabella, Barbara
Farah, Shadia
Peng, Xiaoyu
Burgos-Robles, Anthony Noel
Lim, Seh Hong
Goosens, Ki Ann
Date Issued
July 2016
Journal
Translational Psychiatry
Publisher
Springer Nature
Citation
Gisabella, B., S. Farah, X. Peng, A. Burgos-Robles, S. H. Lim, and K. A. Goosens. “Growth Hormone Biases Amygdala Network Activation after Fear Learning.” Translational Psychiatry 6, no. 11 (November 29, 2016): e960.
Version
Final published version
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.
MIT Department
Massachusetts Institute of Technology. Department of Brain and Cognitive Sciences
McGovern Institute for Brain Research at MIT
Picower Institute for Learning and Memory
Terms of Use
Creative Commons Attribution 4.0 International License
Persistent DSpace Link
DOI of Published Version
https://doi.org/10.1038/tp.2016.203
