Contrasting hippocampal and amygdalar expression of genes related to neural plasticity during escape from social aggression
Publication Type: |
Journal Article |
Year of Publication: |
2012 |
Authors: |
David H. Arendt, Justin P. Smith, Christel C. Bastida, Maneeshi S. Prasad, Kevin D. Oliver, Kathleen M. Eyster, Tangi R. Summers, Yvon Delville, Cliff H. Summers |
Publication/Journal: |
Physiology & Behavior |
Keywords: |
aggression, bdnf, glur1, learned escape, social stress, trkb |
ISBN: |
0031-9384 |
Abstract:
Social subjugation has widespread consequences affecting behavior and underlying neural systems. We hypothesized that individual differences in stress responsiveness were associated with differential expression of neurotrophin associated genes within the hippocampus and amygdala. To do this we examined the brains of hamsters placed in resident/intruder interactions, modified by the opportunity to escape from aggression. In the amygdala, aggressive social interaction stimulated increased BDNF receptor TrKB mRNA levels regardless of the ability to escape the aggressor. In contrast, the availability of escape limited the elevation of GluR1 AMPA subunit mRNA. In the hippocampal CA1, the glucocorticoid stress hormone, cortisol, was negatively correlated with BDNF and TrKB gene expression, but showed a positive correlation with BDNF expression in the DG. Latency to escape the aggressor was also negatively correlated with CA1 BDNF expression. In contrast, the relationship between amygdalar TrKB and GluR1 was positive with respect to escape latency. These results suggest that an interplay of stress and neurotrophic systems influences learned escape behavior. Animals which escape faster seem to have a more robust neurotrophic profile in the hippocampus, with the opposite of this pattern in the amygdala. We propose that changes in the equilibrium of hippocampal and amygdalar learning result in differing behavioral stress coping choices.