Expression of the mu opioid receptor in Drosophila and its effects on trehalose and glycogen when expressed by the AKH neuroendocrine cells
Peptides. 2010-07-01; 31(7): 1383-1389
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Sellami A(1), Isabel G, Veenstra JA.
(1)Université de Bordeaux 1, CNRS, CNIC UMR 5228, 33400 Talence, France.
We made Drosophila which express the mu opioid receptor under control of UAS in
order to inactivate neurons or neuroendocrine cells expressing this receptor with
opioid agonists. However, while exposing flies expressing the mu opioid receptor
in the SIFamide neurons to opioid agonists was expected to induce male-male
courtship behavior, this did not occur. Furthermore, flies which expressed the mu
opioid receptor in the AKH or corazonin endocrine cells increased rather than
decreased trehalose levels and this was independent of opioid agonists. When the
mu opioid receptor is expressed in AKH endocrine cells whole body glycogen also
increases, which is no longer the case if the expression of the AKH gene is
suppressed by RNAi. It appears that mu opioid receptors expressed in AKH or
corazonin endocrine cells are constitutively active and facilitate release of
neurohormones. The simultaneous increase in both glycogen and trehalose in these
flies suggested that they consumed more food. Indeed, when normally fed males are
offered sucrose, those that express this receptor in AKH cells consumed more
sucrose, suggesting that AKH increases the motivation to feed. These
pharmacological effects of the mu opioid receptor are not limited to
neuroendocrine cells; expressing it in the fat body also leads to an increase in
trehalose. Thus in Drosophila the mu opioid receptors appear to change the base
line activity in the cells in which it is expressed, not unlike to what has been
found in transgenic mice expressing receptors activated solely by synthetic
ligands with significant constitutive activity.
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