title: Distribution of GluR1 is altered in the olfactory bulb following neonatal naris occlusion.
abstract: The olfactory system is well suited for studies of glutamate receptor plasticity. The sensory neurons are glutamatergic, and they turn over throughout life, and the olfactory bulb neurons that process their inputs express many of the known glutamate receptor subunits. Neonatal naris occlusion alters olfactory bulb development and the expression of certain neuroactive substances and receptors, at least in part due to loss of the sensory inputs. We therefore postulated that neonatal naris occlusion might alter glutamate receptor expression during postnatal development. Single nares of newborn mice were occluded on postnatal days 1-2, and the distribution of glutamate receptor subunits was evaluated using immunoperoxidase methods. Light microscopic examination on postnatal day 6 failed to reveal adult-like staining of neuronal cell bodies in the olfactory bulbs. By day 12, cell bodies that were immunoreactive (-IR) for the GluR1 subunit were visible in the external plexiform layer (EPL) of both sides. By day 18, many of the GluR1-IR cell bodies could be identified as cell types that had previously been reported to express homomeric GluR1 receptors. Analysis of single, mid-dorsal sections from 18-25-day-old mice showed that the medial EPL of the occluded side had a significantly lower density of these cell bodies. The GluR1 staining of the adjacent mitral cell layer (MCL) was also heavier on the occluded side, but no gross differences in staining for other glutamate receptor subunits were observed. Neonatal naris occlusion therefore appears to provide a new model for studying expression of GluR1 receptors during the development of a discrete population of olfactory bulb neurons.
authors.affiliation: Department of Cellular Biology and Anatomy, Louisiana State University Health Sciences Center, 1501 Kings Highway, Shreveport, Louisiana 71130-3932, USA. khamil@lsuhsc.edu
authors.forename: Kathryn A
authors.initials: KA
authors.lastname: Hamilton
authors.forename: David M
authors.initials: DM
authors.lastname: Coppola
mesh_terms: D000818:Animals; D000831:Animals, Newborn / Q000378:metabolism; D002470:Cell Survival; D005314:Embryonic and Fetal Development / Q000502:physiology; D005260:Female; D007839:Functional Laterality; D007150:Immunohistochemistry; D051379:Mice; D009474:Neurons / Q000378:metabolism / Q000502:physiology; D000857:Olfaction Disorders / Q000378:metabolism; D009830:Olfactory Bulb / Q000254:growth & development / Q000378:metabolism* / Q000473:pathology; D011247:Pregnancy; D018091:Receptors, AMPA / Q000145:classification / Q000378:metabolism*; D012683:Sensory Deprivation / Q000502:physiology*
chemical_list: D018091:Receptors, AMPA