Growth hormone biases amygdala network activation after fear learning
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 t...
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| Format: | Article |
| Language: | en_US |
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Springer Nature
2017
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| Online Access: | http://hdl.handle.net/1721.1/107221 https://orcid.org/0000-0002-6518-1071 https://orcid.org/0000-0002-0010-1595 |
| _version_ | 1826190859188568064 |
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| author | Gisabella, Barbara Farah, Shadia Peng, Xiaoyu Burgos-Robles, Anthony Noel Lim, Seh Hong Goosens, Ki Ann |
| author2 | Massachusetts Institute of Technology. Department of Brain and Cognitive Sciences |
| author_facet | Massachusetts Institute of Technology. Department of Brain and Cognitive Sciences Gisabella, Barbara Farah, Shadia Peng, Xiaoyu Burgos-Robles, Anthony Noel Lim, Seh Hong Goosens, Ki Ann |
| author_sort | Gisabella, Barbara |
| collection | MIT |
| description | 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. |
| first_indexed | 2024-09-23T08:46:24Z |
| format | Article |
| id | mit-1721.1/107221 |
| institution | Massachusetts Institute of Technology |
| language | en_US |
| last_indexed | 2024-09-23T08:46:24Z |
| publishDate | 2017 |
| publisher | Springer Nature |
| record_format | dspace |
| spelling | mit-1721.1/1072212022-09-23T14:28:41Z Growth hormone biases amygdala network activation after fear learning Gisabella, Barbara Farah, Shadia Peng, Xiaoyu Burgos-Robles, Anthony Noel Lim, Seh Hong Goosens, Ki Ann Massachusetts Institute of Technology. Department of Brain and Cognitive Sciences McGovern Institute for Brain Research at MIT Picower Institute for Learning and Memory Gisabella, Barbara Farah, Shadia Peng, Xiaoyu Burgos-Robles, Anthony Noel Lim, Seh Hong Goosens, Ki Ann 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. National Institute of Mental Health (U.S.) (NIMH R01 MH084966) United States. Defense Advanced Research Projects Agency (DARPA grant W911NF-10-1-0059) United States. Army Research Office 2017-03-07T18:20:17Z 2017-03-07T18:20:17Z 2016-07 2016-07 Article http://purl.org/eprint/type/JournalArticle 2158-3188 http://hdl.handle.net/1721.1/107221 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. https://orcid.org/0000-0002-6518-1071 https://orcid.org/0000-0002-0010-1595 en_US http://dx.doi.org/10.1038/tp.2016.203 Translational Psychiatry Creative Commons Attribution 4.0 International License http://creativecommons.org/licenses/by/4.0/ application/pdf Springer Nature Nature |
| spellingShingle | Gisabella, Barbara Farah, Shadia Peng, Xiaoyu Burgos-Robles, Anthony Noel Lim, Seh Hong Goosens, Ki Ann Growth hormone biases amygdala network activation after fear learning |
| title | Growth hormone biases amygdala network activation after fear learning |
| title_full | Growth hormone biases amygdala network activation after fear learning |
| title_fullStr | Growth hormone biases amygdala network activation after fear learning |
| title_full_unstemmed | Growth hormone biases amygdala network activation after fear learning |
| title_short | Growth hormone biases amygdala network activation after fear learning |
| title_sort | growth hormone biases amygdala network activation after fear learning |
| url | http://hdl.handle.net/1721.1/107221 https://orcid.org/0000-0002-6518-1071 https://orcid.org/0000-0002-0010-1595 |
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