• Mallika Padival, Danielle Quinette, and J Amiel Rosenkranz.
• Department of Cellular and Molecular Pharmacology, The Chicago Medical School, Rosalind Franklin University of Medicine and Science, North Chicago, IL 60064, USA.
• Neuropsychopharmacology. 2013 Aug 1;38(9):1748-62.

AbstractChronic stress leads to heightened affective behaviors, and can precipitate the emergence of depression and anxiety. These disorders are associated with increased amygdala activity. In animal models, chronic stress leads to increased amygdala-dependent behaviors, as well as hyperactivity of amygdala neurons. However, it is not known whether increased excitatory synaptic drive after chronic stress contributes to hyperactivity of basolateral amygdala (BLA; comprised of basal, lateral, and accessory basal nuclei) neurons. This study tested whether repeated stress causes an increase in excitatory drive of basal amygdala (BA) neurons in vivo, and whether this is correlated with an increase in the number of dendritic spines and a shift in dendritic distribution. Using in vivo intracellular recordings, this study found that repeated restraint stress caused an increase in the frequency of spontaneous excitatory synaptic events in vivo, which correlated with the number of dendritic spines in reconstructed neurons. Furthermore, parallel changes in the kinetics of the synaptic events and the distribution of spines indicated a more prominent functional contribution of synaptic inputs from across the dendritic tree. The shift in spine distribution across the dendritic tree was further confirmed with the examination of Golgi-stained tissue. This abnormal physiological drive of BA neurons after repeated stress may contribute to heightened affective responses after chronic stress. A reduction in the impact of excitatory drive in the BA may therefore be a potential treatment for the harmful effects of chronic stress in psychiatric disorders.

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