Growth Hormone Regulates Dendritic Spine Density and Neuronal Activity in Amygdala Neurons as a Model for Chronic Stress

Undergraduate #10
Discipline: Biological Sciences
Subcategory: Cell and Molecular Biology

Shadia Farah - Macaulay Honors College at Queens College, CUNY
Co-Author(s): Barbara Gisabella and Ki Ann Goosens, Massachusetts Institute of Technology, Cambridge, MA

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Growth hormone (GH) exerts strong trophic effects in multiple tissues of the body. GH is synthesized within limbic brain areas such as the amygdala, a brain region that regulates emotional memory. Very little is known about how locally synthesized GH regulates emotional processing. Recent studies show that GH may play an important factor in chronic stress because chronic stress increases GH protein expression in the basolateral complex of the amygdala (BL) and GH overexpression dramatically enhances spine density on both primary and secondary branches of BLA neurons. It’s significant to investigate the role GH plays in chronic stress because chronic stress is one of the leading causes of post-traumatic stress disorder (PTSD). Our present project will test the hypothesis test that GH overexpression enhances the ‘size’ of a fear memory by measuring immediate early genes (IEG) expression after fear conditioning. We used an adeno-associated viral vector to overexpress either GH with green florescent protein (GFP) or GFP alone in the BL of adult rats. IEG expression will be quantified by combining confocal imaging with ImageJ analysis. Our results suggest that GH overexpression enhances the size of the fear memory engram, as indicated by increased c-Fos expression in neurons infected with the GH viral vector following fear conditioning in paired mice. This evidence suggests that GH overexpressing neurons are biased to cells that encode for fear memory. Furthermore, we performed an additional control, in which we stressed an unpaired animal group. There was no significant difference in c-Fos levels between control and GH in unpaired animals, showing specificity of the effect of GH on dendritic spines for conditioned fear. These findings support the hypothesis that GH recruits more cells to encode the fear memory engram, providing a mechanism by which chronic stress can contribute to a predisposition for enhanced emotional fear memories associated with PTSD. Future directions will include the quantification of another IEG important for plasticity formation, the ARC protein for comparison with c-Fos.

Funder Acknowledgement(s): This work was supported by the Center for Brains, Minds and Machines (CBMM), funded by NSF STC award CCF-1231216.

Faculty Advisor: Barbara Gisabella,