κ-Opioid receptors in the medial amygdaloid nucleus modulate autonomic and neuroendocrine responses to acute stress

The medial amygdaloid nucleus (MeA) is a key neural structure in triggering physiologic and behavioral control during aversive situations. However, MeA role during stress exposure has not yet been fully elucidated. Thus, in the present study, we investigated the involvement of the MeA opioid neurotransmission in the modulation of autonomic, neuroendocrine and behavioral responses evoked by acute restraint stress (RS). The bilateral microinjection of naloxone (non-selective opioid antagonist) into the MeA potentiated RS-evoked autonomic responses and increased plasma corticosterone levels, in a dose-dependent manner. However, no effects were observed in RS-evoked increases on plasma oxytocin levels and anxiogenic-like behavior. Similar to naloxone, MeA pretreatment with the selective kappa-opioid antagonist (nor-BNI) also enhanced heart rate and corticosterone increases induced by RS, whereas treatment with selective mu- or delta-opioid antagonists did not affect the physiologic and behavioral responses caused by RS. The present results showed MeA kappa-opioid receptors modulate heart rate and corticosterone increases evoked by acute RS, reinforcing the idea of an inhibitory role exerted by MeA during aversive situations. (c) 2020 Elsevier B.V. and ECNP. All rights reserved.

Automated summary

The study found that kappa-opioid receptors in the MeA modulate heart rate and corticosterone increases induced by acute restraint stress, reinforcing the idea of an inhibitory role exerted by MeA during aversive situations.