title: Dopamine activates noradrenergic receptors in the preoptic area.
abstract: Dopamine (DA) facilitates male sexual behavior and modulates aromatase activity in the quail preoptic area (POA). Aromatase neurons in the POA receive dopaminergic inputs, but the anatomical substrate that mediates the behavioral and endocrine effects of DA is poorly understood. Intracellular recordings showed that 100 microm DA hyperpolarizes most neurons in the medial preoptic nucleus (80%) by a direct effect, but depolarizes a few others (10%). DA-induced hyperpolarizations were not blocked by D1 or D2 antagonists (SCH-23390 and sulpiride). Extracellular recordings confirmed that DA inhibits the firing of most cells (52%) but excites a few others (24%). These effects also were not affected by DA antagonists (SCH-23390 and sulpiride) but were blocked by alpha2-(yohimbine) and alpha1-(prazosin) noradrenergic receptor antagonists, respectively. Two dopamine-beta-hydroxylase (DBH) inhibitors (cysteine and fusaric acid) did not block the DA-induced effects, indicating that DA is not converted into norepinephrine (NE) to produce its effects. The pK(B) of yohimbine for the receptor involved in the DA- and NE-induced inhibitions was similar, indicating that the two monoamines interact with the same receptor. Together, these results demonstrate that the effects of DA in the POA are mediated mostly by the activation of alpha2 (inhibition) and alpha1 (excitation) adrenoreceptors. This may explain why DA affects the expression of male sexual behavior through its action in the POA, which contains high densities of alpha2-noradrenergic but limited amounts of DA receptors. This study thus clearly demonstrates the existence of a cross talk within CNS catecholaminergic systems between a neurotransmitter and heterologous receptors.
authors.affiliation: Center for Cellular and Molecular Neurobiology, Research Group in Behavioral Neuroendocrinology, University of Liège, B-4020 Liège, Belgium. Charlotte.Cornil@ulg.ac.be
authors.forename: C A
authors.initials: CA
authors.lastname: Cornil
authors.forename: J
authors.initials: J
authors.lastname: Balthazart
authors.forename: P
authors.initials: P
authors.lastname: Motte
authors.forename: L
authors.initials: L
authors.lastname: Massotte
authors.forename: V
authors.initials: V
authors.lastname: Seutin
mesh_terms: D000200:Action Potentials / Q000187:drug effects / Q000502:physiology; D018674:Adrenergic Antagonists / Q000494:pharmacology; D000818:Animals; D001667:Binding, Competitive / Q000187:drug effects; D003370:Coturnix; D004298:Dopamine / Q000494:pharmacology*; D018491:Dopamine Agonists / Q000494:pharmacology; D018492:Dopamine Antagonists / Q000494:pharmacology; D004299:Dopamine beta-Hydroxylase / Q000378:metabolism; D018756:GABA Antagonists / Q000494:pharmacology; D066298:In Vitro Techniques; D008297:Male; D008564:Membrane Potentials / Q000187:drug effects / Q000502:physiology; D008839:Microelectrodes; D009474:Neurons / Q000187:drug effects / Q000378:metabolism; D009638:Norepinephrine / Q000494:pharmacology; D011301:Preoptic Area / Q000187:drug effects / Q000378:metabolism / Q000502:physiology*; D011941:Receptors, Adrenergic / Q000187:drug effects / Q000378:metabolism*; D009435:Synaptic Transmission / Q000187:drug effects / Q000502:physiology; D013779:Tetrodotoxin / Q000494:pharmacology; D015016:Yohimbine / Q000493:pharmacokinetics
chemical_list: D018674:Adrenergic Antagonists; D018491:Dopamine Agonists; D018492:Dopamine Antagonists; D018756:GABA Antagonists; D011941:Receptors, Adrenergic; D015016:Yohimbine; D013779:Tetrodotoxin; D004299:Dopamine beta-Hydroxylase; D004298:Dopamine; D009638:Norepinephrine