Premium
Involvement of the opioid system in the 17β‐estradiol‐induced enhancement of sucrose intake in ovariectomized rats
Author(s) -
Iida Kurumi,
Kanamori Konomi,
Kondo Sayaka,
Izumi Ayana,
Morimoto Keiko,
Takamata Akira
Publication year - 2019
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.2019.33.1_supplement.553.2
Subject(s) - ovariectomized rat , endocrinology , naltrexone , damgo , medicine , chemistry , nucleus accumbens , opioid , sucrose , saline , agonist , antagonist , opioid receptor , opioid antagonist , receptor , (+) naloxone , pharmacology , estrogen , food science
We previously found that 17β‐estradiol (E2) replacement in ovariectomized rats enhanced progressive increase in 10% sucrose solution intake. In the present study, we hypothesized that the E2‐induced enhancement of sucrose intake is mediated by the opioid system, which is known to play an important role in excessive intake of highly palatable foods. Female Wistar rats were ovariectomized and those rats were assigned to the E2‐treated group (E2 group) or cholesterol‐treated group (Veh group). In the experiment 1, we examined the effect of naltrexone (NTX), an opioid receptor antagonist, on intake of sucrose solution. In this experiment, rats were continuously infused with NTX or saline by an osmotic minipump, and intake of 10% sucrose solution was measured for 14 days. The NTX treatment reversed E2‐induced enhancement of sucrose solution intake. In the experiment 2, we investigated whether the μ‐opioid receptors in the nucleus accumbens (NAc) is involved in the effect of E2‐induced enhancement of sucrose intake. We performed microinjections of a μ‐opioid receptor agonist D‐Ala2, NMe‐Phe4, Glyol5‐enkephalin (DAMGO), NTX or saline into the nucleus accumbens (NAc) in each rat. After microinjections, rats were tested the two‐bottle choice paradigm with 10% sucrose solution and water. Injection of NTX in the NAc reduced sucrose intake in the both groups, and the intake was not different between the groups. These results suggest that the E2‐induced enhancement of sucrose intake is possibly mediated by the opioid system. Also, the opioid receptors in the NAc is a potential site of the action of the E2‐induced enhancement of sucrose intake. Support or Funding Information JPSP KAKENHI #15K12355 and 24500975 to Akira Takamata This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .