Basolateral Amygdala α1-Adrenergic Receptor Suppression Attenuates Stress-Induced Anxiety-Like Behavior and Spine Morphology Impairment on Hippocampal CA1 Pyramidal Neurons

Abstract

The basolateral amygdala (BLA) and hippocampus are part of the limbic fear–anxiety circuit and have also been implicated in the stress response. The BLA is rich in the expression of α1-adrenoceptors. We hypothesized that α1-adrenoceptors in BLA, may modulate stress-induced anxiety-like behavioral responses and hippocampal CA1 pyramidal neuron spine density. α1-Adrenoceptors agonist, phenylephrine, or antagonist, prazosin, were microinjected bilaterally into BLA of male Wistar rats 5 minutes before foot-shock stress. Then, anxiety-like behavioral responses to stress were measured on the Open Field Test (OFT) and on the Elevated Plus-maze (EPM). Also, Golgi-Cox staining was used to investigate the hippocampal CA1 pyramidal neuron spine density. The results showed that four consecutive day stress reduced the open arm time, and open arm entry in the EPM. Intra-BLA injection of prazosin reversed stress-induced anxiogenic-like behaviors. In the OFT stress decreased the center area entries and time, while intra-BLA injection of phenylephrine or prazosin did not alter these parameters. Stress also reduced the dendritic and axonal arborization in hippocampal CA1 pyramidal neurons. Interestingly, intra-BLA infusion of prazosin blocked the reduction in dendritic and axonal arborization induced by foot-shock stress. Taken together, stress produces anxiogenic-like behaviors and hippocampal CA1 pyramidal neurons morphology changes, which may be mediated through the BLA α1-adrenoceptors mechanism.