title: Odor-induced persistent discharge of mitral cells in the mouse olfactory bulb.
abstract: Short-term retention of sensory information in the form of persistent activity of central neurons plays a key role in transforming a brief sensory stimulation into longer-lasting brain responses. The olfactory system uses this transformation for various functional purposes, but the underlying neuronal mechanisms remain elusive. Here, we recorded odor-evoked, single-unit spike responses of mitral and tufted (M/T) cells in the mouse olfactory bulb (OB) under urethane anesthesia and examined the neuronal mechanisms of the persistent discharge (PD) of M/T cells that outlasts the odor stimulus for tens of seconds. The properties of the persistent afterdischarge that occurred after odor stimulation were distinct from those of odor-induced immediate spike responses in terms of the magnitude, odorant specificity, and odorant concentration-response relationship. This suggests that neuronal mechanisms other than prolonged input from olfactory sensory neurons are involved in generating these afterdischarges. Metabotropic glutamate receptor 1 (mGluR1) is expressed in the dendrites of M/T cells and is thought to participate in intraglomerular interactions among M/T cells. In OBs lacking mGluR1, or treated locally with an mGluR1-selective antagonist, the duration of the odor-induced spike responses was significantly lower than that in control OBs, indicating that mGluR1 within the bulbar neuronal circuits participates in the PD generation. These results suggest that neuronal circuits in the OB can actively prolong the odor-induced spike activity of bulbar output neurons and thus transform a brief odor input into longer-lasting activity in the central olfactory system.
authors.affiliation: Department of Physiology, Graduate School of Medicine, The University of Tokyo, 7-3-1 Hongo, Japan.
authors.forename: Hideyuki
authors.initials: H
authors.lastname: Matsumoto
authors.forename: Hideki
authors.initials: H
authors.lastname: Kashiwadani
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Nagao
authors.forename: Atsu
authors.initials: A
authors.lastname: Aiba
authors.forename: Kensaku
authors.initials: K
authors.lastname: Mori
mesh_terms: D000200:Action Potentials / Q000187:drug effects* / Q000235:genetics / Q000502:physiology; D000818:Animals; D001565:Benzoates / Q000494:pharmacology; D004305:Dose-Response Relationship, Drug; D018691:Excitatory Amino Acid Antagonists / Q000494:pharmacology; D005998:Glycine / Q000031:analogs & derivatives / Q000494:pharmacology; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D008954:Models, Biological; D009433:Neural Inhibition / Q000187:drug effects / Q000502:physiology; D009812:Odorants; D009830:Olfactory Bulb / Q000166:cytology*; D009833:Olfactory Pathways / Q000187:drug effects / Q000502:physiology; D018094:Receptors, Metabotropic Glutamate / Q000037:antagonists & inhibitors / Q000172:deficiency / Q000378:metabolism; D012119:Respiration / Q000187:drug effects; D011984:Sensory Receptor Cells / Q000187:drug effects* / Q000502:physiology*; D018709:Statistics, Nonparametric; D013268:Stimulation, Chemical; D013569:Synapses / Q000187:drug effects / Q000235:genetics / Q000378:metabolism
chemical_list: D001565:Benzoates; D018691:Excitatory Amino Acid Antagonists; D018094:Receptors, Metabotropic Glutamate; C104077:metabotropic glutamate receptor type 1; C079694:alpha-methyl-4-carboxyphenylglycine; D005998:Glycine