title: Microglial activation in the developing rat olfactory bulb.
abstract: The development of the olfactory bulb, the primary central relay of the olfactory system, is characterized by a striking susceptibility to alterations in the amount of afferent input. For example, blocking airflow through one half of the nasal cavity during early life results in a number of dramatic changes in the bulb, including increased cell death. Previous studies reveal high levels of microglia in the olfactory bulb. Microglia function as phagocytes, aid in synaptogenesis, and produce important trophic and cytotoxic factors. In response to a number of tissue perturbations, microglia undergo an activation process that includes, among other changes, the up-regulation of complement receptor 3. Interestingly, a previous study reported that naris closure had no effect on microglia in the bulb; however, the research did not distinguish the functional activation state of microglia. We further examined the role of microglia in the normally developing and olfactory-deprived rat bulb using immunohistochemical detection of complement receptor 3 as a measure of microglial activation. Expression of the receptor in the bulb is relatively high during postnatal development, in particular when compared to levels in cortical regions caudal to the olfactory bulb. In addition, naris closure performed on the day after birth (but not after the first postnatal month) increases levels of the receptor in an age and laminar-dependent fashion. The presence of an inducible pool of activated microglia in the olfactory bulb may be important for normal development and contribute to the plethora of changes seen after early olfactory deprivation.
authors.affiliation: Neuroscience Program and Department of Psychology, University of Virginia, Charlottesville, VA 22903, USA.
authors.forename: B K
authors.initials: BK
authors.lastname: Fiske
authors.forename: P C
authors.initials: PC
authors.lastname: Brunjes
mesh_terms: D000818:Animals; D000831:Animals, Newborn; D015703:Antigens, CD; D000951:Antigens, Neoplasm; D000954:Antigens, Surface; D030161:Avian Proteins; D051926:Basigin; D001798:Blood Proteins; D002540:Cerebral Cortex / Q000254:growth & development / Q000473:pathology / Q000503:physiopathology; D003714:Denervation; D016177:Macrophage-1 Antigen / Q000032:analysis / Q000378:metabolism; D008562:Membrane Glycoproteins / Q000032:analysis / Q000494:pharmacology; D017628:Microglia / Q000378:metabolism* / Q000473:pathology*; D009296:Nasal Cavity / Q000601:surgery; D015508:Nasal Obstruction / Q000503:physiopathology; D009830:Olfactory Bulb / Q000254:growth & development* / Q000473:pathology / Q000503:physiopathology*; D051381:Rats; D020318:Rats, Long-Evans
chemical_list: D015703:Antigens, CD; D000951:Antigens, Neoplasm; D000954:Antigens, Surface; D030161:Avian Proteins; D001798:Blood Proteins; C102624:Bsg protein, Gallus gallus; C079432:Bsg protein, rat; D016177:Macrophage-1 Antigen; D008562:Membrane Glycoproteins; D051926:Basigin