Studies of Olfactory System Neural Plasticity: The Contribution of the Unilateral Naris Occlusion Technique

Coppola, David M.

doi:10.1155/2012/351752

Cited by 58 publications

(72 citation statements)

References 118 publications

(161 reference statements)

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“…Based on the current study, UNO, long used as a method of olfactory deprivation in neural plasticity research (Coppola, 2012), also presents itself as a model of brachycephalic airway syndrome in canines and nasal obstruction disorders in humans (Wu et al, 2012). The effects of UNO on the nasal capsule and its contents have obvious implications for the physiological function of these structures including their crucial role in olfaction.…”

Section: Research Articlementioning

confidence: 87%

“…This correction adjusts degrees of freedom based on the variability of a particular sample but the actual number of subjects was invariant across the various measurements. One-tailed tests were justified for comparisons of UNO-treated to normal fossae based on the a priori assumption that the morphology of latter group would be intermediate between open and occluded nasal fossae (Coppola, 2012).…”

Section: Morphometricsmentioning

confidence: 99%

“…In order to test this hypothesis we examined the effects of unilateral naris occlusion (UNO) on turbinate development (Gudden, 1870;Meisami, 1976). UNO is a standard method for producing odor deprivation in studies of sensory plasticity that has profound effects on the developing olfactory system (reviewed by Coppola, 2012). However, this manipulation also causes marked airflow changes in both the occluded and non-occluded (open) nasal fossae (Farbman et al, 1988).…”

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confidence: 99%

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The effects of naris occlusion on mouse nasal turbinate development

Coppola

Craven

Seeger

et al. 2013

Journal of Experimental Biology

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Unilateral naris occlusion, a standard method for causing odor deprivation, also alters airflow on both sides of the nasal cavity. We reasoned that manipulating airflow by occlusion could affect nasal turbinate development given the ubiquitous role of environmental stimuli in ontogenesis. To test this hypothesis, newborn mice received unilateral occlusion or sham surgery and were allowed to reach adulthood. Morphological measurements were then made of paraffin sections of the whole nasal cavity. Occlusion significantly affected the size, shape and position of turbinates. In particular, the nasoturbinate, the focus of our quantitative analysis, had a more delicate appearance on the occluded side relative to the open side. Occlusion also caused an increase in the width of the dorsal meatus within the non-occluded and occluded nasal fossae, compared with controls, and the position of most turbinates was altered. These results suggest that a mechanical stimulus from respiratory airflow is necessary for the normal morphological development of turbinates. To explore this idea, we estimated the mechanical forces on turbinates caused by airflow during normal respiration that would be absent as a result of occlusion. Magnetic resonance imaging scans were used to construct a three-dimensional model of the mouse nasal cavity that provided the input for a computational fluid dynamics simulation of nasal airflow. The simulation revealed maximum shear stress values for the walls of turbinates in the 1 Pa range, a magnitude that causes remodeling in other biological tissues. These observations raise the intriguing possibility that nasal turbinates develop partly under the control of respiratory mechanical forces.

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Section: Research Articlementioning

confidence: 87%

Section: Morphometricsmentioning

confidence: 99%

mentioning

confidence: 99%

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The effects of naris occlusion on mouse nasal turbinate development

Coppola

Craven

Seeger

et al. 2013

Journal of Experimental Biology

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“…Sensory input plays a critical role in the survival of OSNs during postnatal MOE development (Farbman et al, 1988; Stahl et al, 1990; Brunjes, 1994; Coppola et al, 2006). Olfactory sensory deprivation in neonatal mice using unilateral naris occlusion results in a thinner MOE, fewer OSNs, and reduced number of olfactory marker protein (OMP)-positive cells (Coppola et al, 2006; Coppola, 2012). …”

Section: Introductionmentioning

confidence: 99%

Deletion of Type 3 Adenylyl Cyclase Perturbs the Postnatal Maturation of Olfactory Sensory Neurons and Olfactory Cilium Ultrastructure in Mice

Zhang

Yang

Zhang

et al. 2017

Front. Cell. Neurosci.

123

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Type 3 adenylyl cyclase (Adcy3) is localized to the cilia of olfactory sensory neurons (OSNs) and is an essential component of the olfactory cyclic adenosine monophosphate (cAMP) signaling pathway. Although the role of this enzyme in odor detection and axonal projection in OSNs was previously characterized, researchers will still have to determine its function in the maturation of postnatal OSNs and olfactory cilium ultrastructure. Previous studies on newborns showed that the anatomic structure of the main olfactory epithelium (MOE) of Adcy3 knockout mice (Adcy3-/-) is indistinguishable from that of their wild-type littermates (Adcy3+/+), whereas the architecture and associated composition of MOE are relatively underdeveloped at this early age. The full effects of sensory deprivation on OSNs may not also be exhibited in such age. In the present study, following a comparison of postnatal OSNs in seven-, 30-, and 90-day-old Adcy3-/- mice and wild-type controls (Adcy3+/+), we observed that the absence of Adcy3 leads to cumulative defects in the maturation of OSNs. Upon aging, Adcy3-/- OSNs exhibited increase in immature cells and reduction in mature cells along with elevated apoptosis levels. The density and ultrastructure of Adcy3-/- cilia were also disrupted in mice upon aging. Collectively, our results reveal an indispensable role of Adcy3 in postnatal maturation of OSNs and maintenance of olfactory cilium ultrastructure in mice through adulthood.

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“…The initial identification of mRNAs whose abundance depends on odor stimulation can be done by genetically silencing OSNs or by blocking odorant access to the olfactory epithelium. These interventions are highly effective but are not without potential confounding factors (Coppola 2012). First, though naris occlusion is often described as sensory deprivation, it only approximates complete deprivation.…”

Section: Introductionmentioning

confidence: 99%

Activity-Dependent Genes in Mouse Olfactory Sensory Neurons

et al. 2014

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Activity-dependent survival of olfactory sensory neurons (OSNs) may allow animals to tune their olfactory systems to match their odor environment. Activity-dependent genes should play important roles in this process, motivating experiments to identify them. Both unilateral naris occlusion of mice for 6 days and genetic silencing of OSNs decreased S100A5, Lrrc3b, Kirrel2, Slc17a6, Rasgrp4, Pcp4l1, Plcxd3, and Kcnn2 while increasing Kirrel3. Naris occlusion also decreased Eml5, Ptprn, and Nphs1. OSN number was unchanged and stress-response mRNAs were unaffected after 6 days of naris occlusion. This leaves odor stimulation as the most likely cause of differential abundance of these mRNAs, but through a mechanism that is slow or indirect for most because 30-40 min of odor stimulation increased only 3 of 11 mRNAs decreased by naris occlusion: S100A5, Lrrc3b, and Kirrel2. Odorant receptor (OR) mRNAs were significantly more variable than the average mRNA, consistent with difficulty in reliably detecting changes in these mRNAs after 6 days of naris occlusion. One OR mRNA, Olfr855, was consistently decreased, however. These results suggest that the latency from the cessation of odor stimulation to effects on activity-dependent OSN survival must be a week or more in juvenile mice.

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Studies of Olfactory System Neural Plasticity: The Contribution of the Unilateral Naris Occlusion Technique

Cited by 58 publications

References 118 publications

The effects of naris occlusion on mouse nasal turbinate development

The effects of naris occlusion on mouse nasal turbinate development

Deletion of Type 3 Adenylyl Cyclase Perturbs the Postnatal Maturation of Olfactory Sensory Neurons and Olfactory Cilium Ultrastructure in Mice

Activity-Dependent Genes in Mouse Olfactory Sensory Neurons

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