Prolonged behavioral stress enhances synaptic connectivity in the basolateral amygdala.

Recently identified cellular and molecular correlates of stress-induced plasticity suggest a putative link between neuronal remodeling in the amygdala and the development of anxiety-like behavior. Rodent models of immobilization stress, applied for 10 consecutive days, have been reported to enhance anxiety, and also cause dendritic elongation and spine formation in the basolateral amygdala (BLA). Paradoxically, longer exposure to stress, which is also anxiogenic, fails to affect key molecular markers of neuronal remodeling in the BLA. This has raised the possibility of homeostatic mechanisms being triggered by more prolonged stress that could potentially dampen the morphological effects of stress in the BLA. Therefore, we examined the cellular and behavioral impact of increasing the duration of stress in rats. We find that prolonged immobilization stress (PIS), spanning 21 days, caused significant enhancement in dendritic arborization of spiny BLA neurons. Spine density was also enhanced along these elongated dendrites in response to PIS. Finally, this striking increase in synaptic connectivity was accompanied by enhanced anxiety-like behavior in the elevated plus-maze. Thus, we did not detect any obvious morphological correlate of adaptive changes within the BLA that may have been activated by prolonged and repeated application of the same stressor for 21 days. These findings add to accumulating evidence that structural encoding of aversive experiences, through enhanced availability of postsynaptic dendritic surface and synaptic inputs on principal neurons of the BLA, may contribute to the affective symptoms of stress disorders.