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The opioid system of the medial amygdaloid nucleus modulates autonomic and hormonal responses caused by restraint stress in rats
Author(s) -
Fassini Aline,
Scopinho América,
Fortaleza Eduardo,
Resstel Leonardo,
Correa Fernando
Publication year - 2015
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.29.1_supplement.lb715
Subject(s) - corticosterone , stria terminalis , endocrinology , medicine , (+) naloxone , opioid , microinjection , amygdala , heart rate , opioid antagonist , anesthesia , hormone , chemistry , receptor , blood pressure
The medial amydaloid nucleus (MeA) modulates several physiological and behavioral processes, including autonomic changes during aversive situations. The restraint stress (RS) causes significant increase in neuronal activity of the MeA when compared to other amygdaloid nuclei. In addition, the opioid system participates of the mediating cardiovascular responses, including those associated with aversive situations. Based on the facts mentioned above, the hypothesis of this study is that the MeA opioid neurotransmission is involved in the modulation of cardiovascular and endocrine responses evoked by RS. Male Wistar rats (240‐280g) were used. Guide cannulae were implanted bilaterally in the MeA for drug injection and a polyethylene catheter was implanted in the femoral artery for mean arterial pressure (MAP) and heart rate (HR) record. 10 minutes before microinjection of drugs or vehicle into the MeA, rats were subjected to RS. EDTA plasma were used to measured the corticosterone level by ELISA.Increasing doses of the naloxone into the MeA, at dose‐dependent manner, potentiated the increase of MAP (r 2 =0.2096, df=18, P<0.05) and tachycardia (r 2 =0.1704, df=18, P<0.05) and the decrease of tail temperature (r 2 =0.2462, df=18, P<0.05) caused by RS. Also, MeA treatment with naloxone potentiated the increase in corticosterone levels ( F4,22 = 3.49; P=0.24) at 0.03 and 3nmol/100nL of opioid antagonist. In conclusion, opioid neurotransmission mediates the MeA inhibitory influence on restraint‐evoked cardiovascular and endocrine changes. Financial Support: FAPESP, CAPES and FAEPA.