title: Effects of dopaminergic system activation on feeding behavior and growth performance of the sea bass (Dicentrarchus labrax): a self-feeding approach.
abstract: Dopamine is synthesized from l-dopa and subsequently processed into norepinephrine and epinephrine. Any excess neurotransmitter can be taken up again by the neurons to be broken down enzymatically into DOPAC. The effect of dopamine on mammalian food intake is controversial. Mice unable to synthesize central dopamine die of starvation. However, studies have also shown that central injection of dopamine inhibits food intake. The effect of dopaminergic system in the fish feeding behavior has been scarcely explored. We report that the inclusion of l-dopa in the diets results in the activation of sea bass central dopaminergic system but also in the significant increase of the hypothalamic serotonin levels. Dietary l-dopa induces a decrease of food intake and feed conversion efficiency that drives a decline of all growth parameters tested. No behavioral effects were observed after l-dopa treatment. l-dopa treatment stimulated central expression of NPY and CRF. It suggests that CRF might mediate l-dopa effects on food intake but also that CRF neurons lie downstream of NPY neurons in the hierarchical forebrain system, thus controlling energy balance. Unexpectedly, dietary administration of haloperidol, a D2-receptor antagonist, cannot block dopamine effects but also induces a decline of the food intake. This decrease seems to be a side effect of haloperidol treatment since fish exhibited a decreased locomotor activity. We conclude that oral l-dopa inhibits sea bass food intake and growth. Mechanism could also involve an increase of hypothalamic serotoninergic tone.
authors.affiliation: Department of Fish Physiology and Biotechnology, Instituto de Acuicultura de Torre de la Sal, Consejo Superior de Investigaciones Científicas (IATS-CSIC), Castellón, Spain.
authors.forename: Esther
authors.initials: E
authors.lastname: Leal
authors.forename: Begoña
authors.initials: B
authors.lastname: Fernández-Durán
authors.forename: Maria Josep
authors.initials: MJ
authors.lastname: Agulleiro
authors.forename: Marta
authors.initials: M
authors.lastname: Conde-Siera
authors.forename: Jesús Manuel
authors.initials: JM
authors.lastname: Míguez
authors.forename: José Miguel
authors.initials: JM
authors.lastname: Cerdá-Reverter
mesh_terms: D000821:Animal Feed; D000818:Animals; D001492:Bass / Q000502:physiology*; D015306:Biogenic Monoamines / Q000378:metabolism; D003001:Cloning, Molecular; D003346:Corticotropin-Releasing Hormone / Q000235:genetics / Q000378:metabolism; D004298:Dopamine / Q000502:physiology*; D015259:Dopamine Agents / Q000494:pharmacology; D018492:Dopamine Antagonists / Q000494:pharmacology; D065127:Dopamine D2 Receptor Antagonists; D004305:Dose-Response Relationship, Drug; D005247:Feeding Behavior / Q000502:physiology*; D005260:Female; D015870:Gene Expression / Q000187:drug effects / Q000502:physiology; D006128:Growth / Q000502:physiology*; D006220:Haloperidol / Q000494:pharmacology; D007980:Levodopa / Q000494:pharmacology; D008297:Male; D009479:Neuropeptides / Q000096:biosynthesis / Q000235:genetics
chemical_list: D015306:Biogenic Monoamines; D015259:Dopamine Agents; D018492:Dopamine Antagonists; D065127:Dopamine D2 Receptor Antagonists; D009479:Neuropeptides; D007980:Levodopa; D003346:Corticotropin-Releasing Hormone; D006220:Haloperidol; D004298:Dopamine