Atypical endogenous opioid systems in mice in relation to an auto-addiction opioid model of anorexia nervosa.

Abstract:

:We have proposed that the atypical opioid system in the mouse may be representative of that in the anorexia nervosa patient and may account for a biological predisposition to the disorder. This is in the context of our auto-addiction model of anorexia nervosa in which endogenous opioids play a critical role in its etiology. Morphine activation of the endogenous opioid systems increases food intake and causes sedation in most species, including normal humans and rats. In contrast in BALB/C mice, morphine causes anorexia and hyperactivity, which we suggest may be true in the anorexia nervosa patient. A variety of atypical opioid systems have been demonstrated in different mouse strains, based on other responses. The present study examines these strains with reference to the responses relevant to our anorexia nervosa model. Three patterns are described--anorexia with hyperactivity (BALB/C and C57BL/6J mice), anorexia without hyperactivity (DBA/J mice), and a biphasic curve with hyperphagia at low doses and anorexia and hyperactivity at higher doses (CF-1 mice). Only female mice were used. These atypical opioid systems may reflect a spectrum of biological predispositions to the disorder. These strain differences may also provide useful correlations of the genetic determinants of various opiate responses and provide useful comparisons in characterizing the essential features responsible for the atypical responses.

journal_name

Life Sci

journal_title

Life sciences

authors

Marrazzi MA,Mullings-Britton J,Stack L,Powers RJ,Lawhorn J,Graham V,Eccles T,Gunter S

doi

10.1016/0024-3205(90)90521-r

subject

Has Abstract

pub_date

1990-01-01 00:00:00

pages

1427-35

issue

16

eissn

0024-3205

issn

1879-0631

pii

0024-3205(90)90521-R

journal_volume

47

pub_type

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