title: Dopaminergic modulation of mitral cell activity in the frog olfactory bulb: a combined radioligand binding-electrophysiological study.
abstract: Dopamine content in the amphibian olfactory bulb is supplied by interneurons scattered among mitral cells in the external plexiform/mitral cell layer. In mammals, dopamine has been found to be involved in various aspects of bulbar information processing by influencing mitral cell odour responsiveness. Dopamine action in the bulb depends directly on the localization of its receptor targets, found to be mainly of the D2 type in mammals. The present study assessed, in the frog, both the anatomical localization of D2-like, radioligand-labelled receptors of dopamine and the in vivo action of dopamine on unitary mitral cell activity in response to odours delivered over a wide range of concentrations. The [125I]iodosulpride-labelled D2 binding sites were visualized on frozen sagittal sections of frog brains by film radioautography. The sites were found to be restricted to the external plexiform/mitral cell layer; other layers of the olfactory bulb were devoid of specific labelling. Electrophysiological recordings of mitral unit activity revealed that dopamine or its agonist apomorphine induced a drastic reduction of spontaneous firing rate of mitral cells in most cases without altering odour intensity coding properties of these cells. Moreover, pre-treatment with the D2 antagonist eticlopride blocked the dopamine-induced reduction of mitral cell spontaneous activity. In the frog olfactory bulb, both anatomical localization of D2-like receptors and functional data on dopamine involvement in information processing differ from those reported in mammals. This suggests a phylogenetic evolution of dopamine action in the olfactory bulb. In the frog, anatomical data perfectly corroborate electrophysiological results, together strongly suggesting a direct action of dopamine on mitral cells. In a physiologically operating system, such an action would result in a global improvement of signal-to-noise ratio.
authors.affiliation: Laboratoire de Physiologie Neurosensorielle, Universite Claude Bernard and CNRS, Villeurbanne, France.
authors.forename: P
authors.initials: P
authors.lastname: Duchamp-Viret
authors.forename: V
authors.initials: V
authors.lastname: Coronas
authors.forename: J C
authors.initials: JC
authors.lastname: Delaleu
authors.forename: E
authors.initials: E
authors.lastname: Moyse
authors.forename: A
authors.initials: A
authors.lastname: Duchamp
mesh_terms: D000818:Animals; D001058:Apomorphine / Q000494:pharmacology; D004298:Dopamine / Q000494:pharmacology* / Q000502:physiology; D018491:Dopamine Agonists / Q000494:pharmacology*; D018492:Dopamine Antagonists / Q000494:pharmacology*; D004594:Electrophysiology; D008564:Membrane Potentials / Q000187:drug effects; D009474:Neurons / Q000166:cytology / Q000187:drug effects / Q000502:physiology*; D009812:Odorants; D009830:Olfactory Bulb / Q000166:cytology / Q000502:physiology*; D011869:Radioligand Assay; D011895:Rana ridibunda; D011930:Reaction Time / Q000187:drug effects; D017448:Receptors, Dopamine D2 / Q000187:drug effects / Q000502:physiology*; D012457:Salicylamides / Q000494:pharmacology
chemical_list: D018491:Dopamine Agonists; D018492:Dopamine Antagonists; D017448:Receptors, Dopamine D2; D012457:Salicylamides; C045989:eticlopride; D001058:Apomorphine; D004298:Dopamine