Expression of the mu opioid receptor in Drosophila and its effects on trehalose and glycogen when expressed by the AKH neuroendocrine cells

Abstract

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.