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Abstract
Imbalances in dopaminergic signaling during development have been indicated as part of the underlying neurobiology of several psychiatric illnesses, including schizophrenia, major depression, bipolar disorder, and food addiction. Yet, how transient manipulation of dopaminergic signaling influences long-lasting behavioral consequences, or if these modifications can induce inheritable traits, it is still not understood. In this study, we used the Drosophila melanogaster model to test if transient pharmacological activation of the dopaminergic system leads to modulations of feeding and locomotion in adult flies. We observed that transient administration of a dopaminergic precursor, levodopa, at 6 h, 3 days or 5 days post-eclosion, induced overfeeding behavior, while we did not find significant effects on locomotion. Moreover, this phenotype was inherited by the offspring of flies treated 6 h or 3 days post-eclosion, but not the offspring of those treated 5 days post-eclosion. These results indicate that transient alterations in dopaminergic signaling can produce behavioral alterations in adults, which can then be carried to descendants. These findings provide novel insights into the conditions in which environmental factors can produce transgenerational eating disorders.
Highlights
The dopaminergic system is involved in the pathophysiology of several psychiatric illnesses, such as schizophrenia [1], major depression [2], and bipolar disorder [3]
We investigate if transient manipulation of dopaminergic pathways by levodopa treatment after eclosion is able to induce inheritable feeding-behavior alterations in the Drosophila melanogaster model
Our results indicate that transitory dopaminergic imbalances can produce feeding disorders, which can be inherited by the offspring of parents affected during early adult stages
Summary
The dopaminergic system is involved in the pathophysiology of several psychiatric illnesses, such as schizophrenia [1], major depression [2], and bipolar disorder [3]. Transient disturbances in dopamine signaling during development have been implicated as a possible origin to maladaptive neural mechanisms, which in turn could generate aberrant behaviors [4]. Activation of dopaminergic neurons during the developmental stages of Drosophila melanogaster models were shown to cause adult phenotypes related to cognitive impairments, such as alterations in sensory responsiveness and locomotion [5,6]. Mounting evidence indicates that imbalances of the dopaminergic reward system facilitates the emergence of compulsive responses to food, contributing to food addiction and obesity through modulation of reinforcement and motivation [7,8,9,10]. The link between developmental dopaminergic disturbances and subsequent alterations in eating behavior remains surprisingly unexplored. One of the first documented cases of such transgenerational influence was the Dutch Hunger Winter Study, which showed that children
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