Angiontensinergic Receptors in the Medial Amygdaloid Nucleus Is Involved in Anxiogenic‐Like Effect Evoked by Emotional Stress in Rats

Abstract

The medial amygdaloid nucleus (MeA) is part of limbic circuit implicated in responses to stress. Besides, angiotensinergic neurotransmission has been described as a prominent neurochemical mechanism involved in stress‐evoked physiological and behavioral responses. However, the involvement of angiotensinergic neurotransmission within the MeA in behavioral responses evoked by exposure to aversive threats has never been investigated. Therefore, the aim of this study was to investigate the involvement of angiotensinergic neurotransmission within the MeA in anxiogenic‐like effect evoked by an acute session of restraint stress in rats. For this, male Wistar rats (240g–260g) had cannula‐guide bilaterally implanted into the MeA. The restraint stress was performed by placing the animals in a plastic cylindrical tube for 60 minutes. Independent group of animals received bilateral microinjections into the MeA of angiotensin II (0.05nmol/100nL), the selective AT1receptor antagonist losartan (1nmol/100nL), the selective AT2receptor antagonist PD123319 (0.05nmol/100nL), angiotensin 1–7 (0.05nmol/100nL), the selective Mas receptor antagonist A‐779 (0.1nmol/100nL) or vehicle (saline, 100nl)10 min before the onset of the restraint stress session. Immediately after the end of the restraint session, the anxiety‐like behavior was assessed in the elevated plus maze (EPM). Animals of naïve group (non‐stressed) were tested in the EPM together with stressed animals. We identified that restraint stress decreased the percentage of time spent (F(6,63)=7.98; P<0.0001) and number of entries (F(6,63)=7.40; P<0.0001) in the open arms of the EPM in the vehicle‐treated animals, when compared with naïve animals. Restraint did not affect the number of entries in the enclosed arms (F(6,63)=0.30; P>0.05) and the time spent in the center (F(6,63)=0.85; P>0.05). MeA treatment with either losartan, angiotensin II or angiotensin 1–7 inhibited the restraint‐evoked decrease in the percentage of time spent (P<0.05) and number of entries (P<0.05) in the open arms. Microinjection of either PD123319 (time: P<0.001; entries: P<0.0007) or A‐779 (time: P<0.008; entries: P<0.01) did not affect the decrease in the exploration of the EPM open arms evoked by restraint stress. In conclusion, our results indicate that AT1receptors within the MeA is involved in anxiogenic‐like effect of emotional stress. Besides, present data suggest that activation of the Mas receptor within the MeA inhibits this behavioral response.Support or Funding InformationFAPESP, CNPq and PADC‐FCF/UNESPThis abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.