Sensory Deafferentation Transsynaptically Alters Neuronal GluR1 Expression in the External Plexiform Layer of the Adult Mouse Main Olfactory Bulb

Abstract

Altered distribution of the alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA) receptor subunit GluR1 has been linked to stimulation-dependent changes in synaptic efficacy, including long-term potentiation and depression. The main olfactory bulb (OB) remains plastic throughout life; how GluR1 may be involved in this plasticity is unknown. We have previously shown that neonatal naris occlusion reduces numbers of interneuron cell bodies that are immunoreactive for GluR1 in the external plexiform layer (EPL) of the adult mouse OB. Here, we show that immunoreactivity of mouse EPL interneurons for GluR1 is also dramatically reduced following olfactory deafferentation in adulthood. We further show that expression of glutamic acid decarboxylase (GAD) 65, 1 of 2 GAD isoforms expressed by adult gamma-aminobutyric acidergic interneurons, is reduced, but to a much smaller extent, and that in double-labeled cells, immunoreactivity for the Ca(2+)-binding protein parvalbumin (PV) is also reduced. In addition, GluR1 expression is reduced in presumptive tufted cells and interneurons that are negative for GAD65 and PV. Consistent with previous reports, sensory deafferentation resulted in little neuronal degeneration in the adult EPL, indicating that these differences were not likely due to death of EPL neurons. Together, these results suggest that olfactory input regulates expression of the GluR1 AMPA receptor subunit by tufted cells that may in turn regulate GluR1 expression by interneurons within the OB EPL.

Mature and Precursor Brain-Derived Neurotrophic Factor Have Individual Roles in the Mouse Olfactory Bulb

“…Alternatively, activated-caspase 3 may be a mechanism by which sensory input, or lack thereof, regulates synapse and dendrite plasticity [58]. Indeed, after sensory input loss the OB undergoes extensive synaptic remodeling and neurite pruning as measured at the histological, receptor and physiological level [6], [13], [30], [61]–[63]. Furthermore, proliferating neurons of the olfactory bulb, including those in the glomerular layer, briefly express activated-caspase 3 [64].…”

The Olfactory System as a Puzzle: Playing With Its Pieces

“…There is a decrease in the expression levels of tyrosine hydroxylase, dopamine, substance P, neuronal nitric oxide synthase—and its related NADPH‐diaphorase activity—and calbindin D‐28K (Nadi et al, ; Kawano and Margolis, ; Baker et al, ; Kream et al, ; Leo et al, ; Weruaga et al, ). The immunoreactivity of the mouse external plexiform layer interneurons for GluR1 is also dramatically reduced following olfactory deafferentation in adulthood (Hamilton et al, ). Recently, it has been demonstrated that both olfactory deprivation and olfactory deafferentation reduce GAD67 protein and the number of short‐axon cells expressing GAD67 in the OB (Parrish‐Aungst et al, ).…”

Olfactory sensory deprivation increases the number of proBDNF-immunoreactive mitral cells in the olfactory bulb of mice

“…The origin of the oEPL BDNF-ir fibers described here is not clear, but may belong to secondary dendrites of middle-tufted cells since these dendrites ramify into the superficial EPL [27]. Indeed, Hamilton et al (2008) have recently shown that middle-tufted cells may undergo trophic changes after adult olfactory-sensory deprivation induced by deafferentation [16]. Our data may, therefore, provide preliminary evidence for a functional segregation within the EPL.…”