Study On The Effect Of Chronic Immobilization Stress On The Expression Of GABA_B Receptor In Amygdala

As a key part of the limbic system in the mammalian brain, the amygdala complex plays a vital role in the formation and expression of emotion. After receiving and integrating the dangerous information from its neighboring areas such as hippocampus and thalamus, the amygdala transfers these signals to the downstream brain areas to evoke appropriate expression of fear and anxiety. Under resting state, the inhibitory tone inside amygdala is particularly high relative to the surrounding brain areas. Upon stress, this highly inhibitory tone is rapidly removed, enabling the signal transfer from amygdala to the downstream areas and resulting in the expression of fear and anxiety. It has been generally recognized that the prolonged stress makes the amygdala hyperactive and lead to the persistent expression of anxiety. However, the underlying neurobiological mechanisms remain largely unknown. GABABR is one of the key receptors by which GAB A mediates its inhibitory role in the CNS. We have recently shown that activation of GABABR in amygdala selectively suppresses the synaptic transmission between the adjacent areas and amygdala projection neurons, which helps to maintain the highly inhibitory tone in amygdala. On the other hand, the mice with genetic deletion of GABABR are more anxious, highlighting a role of GABABR in limiting the expression of anxiety. However, it is thus far unknown whether GABABR in the amygdala is involved in the anxiety caused by chronic stress. To test this scenario, we establish the mice model of chronic immobilization stress (CIS) and study the potential impact of CIS on the expression and function of GABABR in amygdala by using combined approaches of behavior, immunochemistry and electrophysiology. We find that the CIS makes mice hyperactive and more anxious while leaving their exploration nature unaffected. Meanwhile, the GBR1expression in amygdala is moderately reduced while that of GBR2is increased dramatically. After10days recovery, the expression of GBR1in the amygdala remains unaltered and the GBR2declines remarkably. Beside these, CIS does not affect the GABABR currents in the lateral part of amygdala. The above results provide valuable experimental data to elucidate the potential influence of CIS on the expression of GABABR in the amygdala and may help for the prevention and treatment of anxiety and other mental disorders.