Contrasting hippocampal and amygdalar expression of genes related to neural plasticity during escape from social aggression

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.

Depressive behavior and activation of the orexin/hypocretin system.

“…Depression restructures the brain in both size and function (Drevets, 2000;Lakshminarasimhan & Chattarji, 2012;Pittenger & Duman, 2008), but perhaps endogenous systems (such as orexin) modify specific brain regions differentially. Although further experiments would have to be carried out to confirm that these areas have altered orexin signaling, the differences measured in orexinergic expression in the hippocampus and amygdala are in line with other work that points to opposing effects between these two areas (Arendt et al, 2012;Lakshminarasimhan & Chattarji, 2012). This work elucidates some possible mechanisms for orexin to alter plasticity in these specific brain regions associated with depression.…”

Nuance and behavioral cogency: How the Visible Burrow System inspired the Stress-Alternatives Model and conceptualization of the continuum of anxiety

“…1D). The latency to use the escape route was similar to all other experiments using this model: slow during the first trial, and significantly faster each day thereafter [86]. The total amount of aggression received by the test animal did not vary depending on the possibility to escape, however the latency to contact in these interactions was significantly longer when escape was available.…”

Cross-training in birds: cold and exercise training produce similar changes in maximal metabolic output, muscle masses and myostatin expression in house sparrows,Passer domesticus

“…Slopes and efficiencies for each gene were: GAPDH (−3.46, 94.6%), myostatin (−3.52, 92.4%), TLL-1 (−3.34, 99.4%), TLL-2 (−3.42, 95.9%), respectively. We quantified changes in mRNA expression using the 2 −ΔΔCT method (Livak and Schmittgen, 2001;Arendt et al, 2012), comparing all samples to a reference sample. We used the mean value for all seasons for each tissue for each gene as the reference sample and set the value for this reference sample equal to 1.…”