Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “OLFACTORY NERVE”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 811 records · Page 45Linked to original sources
PubMed2006

Posttraumatic olfactory loss.

Head injury is the leading cause of posttraumatic anosmia. Complete or partial loss of olfactory function may occur when the nasal passages are blocked, olfactory nerves are injured or there are contusions or hemorrhages in olfactory centers of the brain. Evaluation of patients with posttraumatic olfactory loss should include a physical examination by the otolaryngologist. Nasal endoscopy and radiological studies should be performed as well as olfactory function tests to determine the degree and type of olfactory impairment. Although treatment options may be limited, physicians should provide information and counseling regarding the risks and hazards associated with loss of olfactory function. For some individuals such as cooks, firefighters, and research scientists, an assessment of vocational activities should be performed prior to reentry into the workplace. Individuals with impaired olfactory function may be unable to detect important warning signs such as gas leaks, volatile chemical fumes and fires and therefore place themselves and coworkers at an increased risk for serious injury or death.

Craniocerebral Trauma↗
PubMed1975

Quantitative observations on the nasal epithelia and olfactory innervation in bats. Suggested design mechanisms for the olfactory bulb.

The nasal epithelia of two species of bats were quantified with respect to relative surface areas and olfactory epithelial volumes. In the macrosmatic Aribeus jamaicensis 55.9% of the nasal cavity surface was covered by olfactory epithelium (232.4 mm2), in contrast to only 28.9% in the microsmatic Myotis lucifugus (36.4 mm2). The roles of the various nasal epithelia have been discussed as they may relate to olfaction, respiration and echolocation. In the olfactory bulbs of both species, the estimated concentration of mitral cells approximated at 2,500/mm2 compared to an olfactory nerve concentration of 5/mm2. In Artibeus, calculated total volume of olfactory epithelium was on the order of 16 times greater than in Myotis, and Artibeus' olfactory bulb diameter was twice as great. These findings, together with previously published surface, volume and physiological relationships, suggest a developmental design mechanism for an olfactory bulb in which the number of olfactory receptors increases some 450-fold above an initially established ratio of 2:1 between receptors and mitral cells. Key governing factors could be requisite mechanical rigidity of the cribriform plate of the ethmoid bone and response thresholds of higher brain centers.

Animals↗
PubMed2005

Adenovirus-mediated gene transfer in olfactory epithelium and olfactory bulb: a long-term study.

OBJECTIVES: We sought to study the spatiotemporal gene expression mediated by adenoviral vector in the olfactory pathways. METHODS: The replication-defective adenoviral vector AxCALacZ, which encodes the enzyme Escherichia coli beta-galactosidase, was applied to mouse olfactory epithelium by intranasal instillation. RESULTS: The LacZ gene product, beta-galactosidase, was expressed not only in the olfactory receptor neurons and their axons, but also in the olfactory bulbs. The first evidence of anterograde labeling was observed at postinfection day (PID) 2. At PID 3, beta-galactosidase was strongly expressed in olfactory nerve axons, as well as their terminal glomeruli, in the olfactory bulbs. beta-Galactosidase expression persisted up to PID 90, and there was a significant decrease in the number of labeled neurons at PID 30. CONCLUSIONS: These results suggest possible long-term effects of adenovirus-mediated gene transfer on the olfactory neurons, as well as the olfactory bulbs.

Adenoviridae↗
PubMed1992

Differential localization of G proteins, Gi and Go, in the olfactory epithelium and the main olfactory bulb of the rat.

The immunohistochemical localization of proteins Gi1 (plus Gi3). Gi2 and Go was studied in the olfactory epithelium and the main olfactory bulb of rats, using purified antibodies to the respective alpha subunits and beta gamma subunits of these G proteins. In the olfactory epithelium, only a restricted population of olfactory cells was immunopositive for Gi2 alpha, but others were not. The immunoreactivity for Gi1 alpha/Gi3 alpha was not observed. The olfactory epithelium was immunopositive for both Go alpha and beta gamma, but its apical surface was immunopositive only for beta gamma. In the main olfactory bulb, all layers were intensely immunopositive for Go alpha and beta gamma but weakly for Gi2 alpha. In contrast to the negative or weak immunostainings in the olfactory nerve fiber layer and glomeruli, the molecular and the internal granular layers were intensely immunopositive for Gi1 alpha/Gi3 alpha. These findings suggest the functional difference among Gi1/Gi3, Gi2 and Go in the signal transduction in the olfactory system.

Animals↗
PubMed2000

Deafferentation-induced changes in the olfactory bulb of adult zebrafish.

The influence of the olfactory organ on maintenance of olfactory bulb structure was examined in zebrafish, using peripheral deafferentation. This fish provides a model in which the olfactory organ is easily accessible for removal, the animals easily survive the surgery, and the olfactory bulbs are small enough to allow rigorous analysis of the resulting effects. Unilateral olfactory organ ablations were performed on anesthetized adult zebrafish using a small-vessel cautery iron. Fish were allowed to survive for 1, 3, or 6 weeks following the procedure. Analysis of deafferented animals revealed that most, if not all, of the olfactory organ was missing on the ablated side, and the structure did not regenerate. The morphology of the olfactory bulb was affected notably by the removal of its primary afferent innervation. The olfactory nerve layer was diminished at 1 week and absent by 3 weeks post-deafferentation. At all of the survival times the deafferented bulb appeared significantly smaller at the gross level, and there was a statistically significant effect on bulb size and cell number after 6 weeks. Tyrosine hydroxylase expression, as revealed by immunohistochemistry, was decreased noticeably on the ablated side. In conclusion, the olfactory organ is important in the preservation of normal olfactory bulb anatomy and neurochemistry in adult zebrafish. Thus, the influence of the periphery does not end with the formation of the mature olfactory bulb.

Animals↗
PubMed1995

Expression of the amyloid protein precursor of Alzheimer's disease in the developing rat olfactory system.

The expression of the amyloid protein precursor (APP) of Alzheimer's disease (AD) was examined in the olfactory system of the developing rat. Two monoclonal antibodies were used to detect APP: Alz-90, which specifically recognizes APP, and 22C11 which recognizes both APP and the structurally related protein APLP-2. Very similar patterns of immunoreactivity were observed with both antibodies. APP immunoreactivity was first detected in a subpopulation of olfactory epithelial cells at embryonic day 16 (E16), at a time when primary sensory olfactory axons are first beginning to pierce the glia limitans of the olfactory bulb. At E16, there were more olfactory receptor neurons which expressed APP than the olfactory marker protein (OMP), indicating that some APP-containing neurons were not fully mature. Between E16 and postnatal day 8 (P8), there was a marked increase in the number of primary sensory olfactory neurons expressing APP. In the olfactory bulb, APP was first detected in the mitral cell layer at E18, at a time when synapses are first beginning to form between the dendrites of these cells and primary sensory axons. The level of APP detected within mitral cell perikarya decreased after birth and could no longer be detected between P3 and P8. This indicated that once synaptic connections had been initiated within olfactory glomeruli, the expression of APP within the mitral cells was down-regulated. High levels of APP were, however, detected within the olfactory nerve fiber layer and glomeruli between P3 and P8. The results demonstrate that APP expression in the olfactory system is coordinately regulated with the major periods of synaptogenesis.(ABSTRACT TRUNCATED AT 250 WORDS)

Alzheimer Disease↗
PubMed2000

Sensory deafferentation and olfactory bulb morphology in the zebrafish and related species.

The zebrafish, Danio rerio, has become an important model species for examining olfactory system structure and function, yet little is known about developmental changes in olfactory bulb morphology from embryo to adult. The present study examined both normal growth and the effects of deafferentation on the bulb from hatching to adulthood. In young animals, the bulb is small relative to body size and has a higher percentage of its volume occupied by incoming olfactory nerve fibers. Young animals are also more affected by sensory deafferentation. Olfactory rosette removal resulted in more than 50% reductions in laminar volumes, indicating that sensory input is important during periods of rapid development. In addition, three closely related species were examined to compare how differing bulb morphology might influence the effects of bulb manipulation. The cherry barb, Barbus (=Puntius) titteya, and giant danio, Danio aequipinnatus, have larger bulbs and laminar volumes relative to body size than the zebrafish or scissortail rasbora, Rasbora trilineata. Both are also more affected by deafferentation, with at least a 35% reduction in laminar sizes in many of the bulb layers. The studies are discussed in terms of the importance of the olfactory system to each species and are also compared to the effects of sensory manipulations in other animals.

Animals↗
PubMed1984

The olfactory nervous system of the old world monkey.

This paper reviews work on olfactory function performed in the author's laboratory over the last 10 years. The following aspects of this work are covered. Neocortical olfactory areas were studied in old world monkeys. Olfactory responses were found in the lateroposterior and centroposterior portions of the orbitofrontal cortex (LPOF and CPOF). The routes of the olfactory nerve pathways to the LPOF and the CPOF were examined. An olfactory pathway to the lateral hypothalamic area (LHA) was also studied. Using unanesthetized monkeys, information processing of odors was studied in the OB, PPF-MA, LPOF, MDmc, CPOF, and LHA. In the LPOF and LHA, half or more of the cells responded differentially to one odor. We have thus been able to clearly demonstrate discrimination of odors at the cell level in these areas.

Anesthesia, General↗
PubMed2000

[Description and analysis of olfactory disorders after head trauma. Review of the literature].

Olfactory disorders subsequent to head trauma can raise medicolegal problems when the olfactory deficit occurs after a work accident or a traffic accident and also raises the problem of psychological and functional tolerance when the patient consults late for a therapeutic solution. We studied the epidemiology of olfactory disorders after head trauma. Such disorders have been recognized since the XIX(th) century. Several studies have attempted to determine the prevalence of olfactory sequelae after head trauma. We then describe the pathophysiology of these lesions and emphasize that the degree of severity is related with the gravity of the head trauma and that the prevalence of these disorders varies considerably depending on the site of the trauma. Mechanisms which can lead to lesions of the olfactory system include, damage to the olfactory nerve bundles, naso-sinus lesions, or lesions of the cerebral olfactory centers. Brain MRI in anosmic patients after head trauma allows a visualization of intracranial lesions. The degree of reversibility of olfactory disorders after head trauma is imperfectly evaluated and discordant results have been reported. Some authors consider loss of olfaction is definitive. Others suggest an improvement in olfaction the year following head trauma. We reviewed the literature on these different elements. Expert opinions concerning patients complaining of olfactory disorders should relate this disorder to the initial trauma and determine the personal and occupational impact of the deficit. Attribution of cause must take into account all the clinical, radiological and psycho-olfactory factors.

Brain Damage, Chronic↗
PubMed1992

Effects of lesions of the optic nerve, optic tectum and nervus terminalis on rod precursor proliferation in the goldfish retina.

Teleost retinas grow throughout life by proliferation of neuroblasts at the retinal margin and dedicated rod precursors in the outer nuclear layer. Mechanisms regulating this proliferation are largely unknown. Previous investigators observed that rod precursor replication, as detected by incorporation of radioactive thymidine into cells of the outer nuclear layer, is enhanced after optic nerve crush. We attempted to determine whether this was due to severing of the retinopetal (nervus terminalis, n.t.) or retinofugal (retinal ganglion cell) axons in the optic nerve of the goldfish, Carassius auratus. In the first series of experiments, we ablated unilaterally the optic nerve, olfactory bulb (containing n.t. ganglia), or optic tectum (containing retinal ganglion cell axons and n.t. collaterals). Rod precursor proliferation increased dramatically in both retinas as soon as 5 days after surgery; in addition, the numbers of dividing cells were greater in the ipsilateral retina 10-15 days after optic nerve crush or tectal ablation and in the contralateral retina 20-25 days after olfactory bulb ablation. These observations are not accounted for by the known projections of retinal ganglion cells, but are consistent with the projections of the n.t. In the second series of experiments, n.t. projections to the brain and retina were severed bilaterally 7-8 weeks before the unilateral optic nerve crush or hemitectal ablation. Rod precursor proliferation increased as before, but the quantities of dividing cells were always equal in both retinas. We conclude that the n.t. may modulate rod proliferation locally and that injury to (some) brain regions may cause release of mitogens that affect rod precursors in both retinas.

Animals↗
PubMed2002

The role of serine proteases and serine protease inhibitors in the migration of gonadotropin-releasing hormone neurons.

BACKGROUND: Mechanisms regulating neuronal migration during development remain largely undefined. Extracellular matrix cues, target site released factors, and components of the migratory neurons themselves are likely all coordinated in time and space directing neurons to their appropriate locations. We have studied the effects of proteases and their inhibitors on the extracellular matrix and the consequences to the migration of gonadotropin releasing hormone (GnRH) neurons in the embryonic chick. Chick GnRH neurons differentiate in the olfactory epithelium, migrate along the olfactory nerve and enter the forebrain. The accessibility of this coherent cell group make it amenable for studying protease/inhibitor roles in migratory processes. RESULTS: Affigel blue beads were used to deliver a serine protease inhibitor, protease nexin-1 (PN-1), and a target protease, trypsin, to the olfactory epithelium coincident with initiation of GnRH neuronal migration. PN-1 inhibited neuronal migration while trypsin accelerated their transit into the CNS. Prior to initiation of migration, neither PN-1 nor trypsin altered the timing of neuronal exit. Trypsin did, however, accelerate the timing of neuronal crossing into the nerve-forebrain junction. CONCLUSIONS: These data support the hypothesis that protease activity modulates neuronal movements across barriers. Moreover, the data suggest, for the first time, that aspects of GnRH neuronal migration may be cell autonomous but modulated by ECM alterations.

Amyloid beta-Protein Precursor↗
PubMed1996

Distribution of FMRFamide-like immunoreactivity in the brain and pituitary of Rana esculenta during development.

Developmental aspects of the distribution of FMRFamide (Phe-Met-Arg-Phe-NH2) immunoreactivity (ir) were investigated by indirect immunofluorescence in the brain, pituitary and terminal nerve of the frog, Rana esculenta. Soon after hatching. FMRFamide neurons were found in the proximal terminal nerve, mediobasal olfactory bulb, caudal dorsolateral pallium, diagonal band of Broca, anterior preoptic area, suprachiasmatic area, thalamus, infundibulum, and developing pituitary. FMRFamide fibers were present in the olfactory epithelium, terminal nerve, olfactory bulbs, dorsal and midventral telencephalon, epiphysis, mediolateral thalamus, pretectal gray, optic tectum, infundibulum, posterior interpeduncular nucleus-tegmentum area, and rostral rhombencephalon. During successive developmental stages, ir neurons were no longer observed in the dorsal telencephalon and pituitary. In late larval stages, ir neurons appeared in the medial septal area, and ir fibers in the cerebellum and torus semicircularis. At the same time, the frequency of ir neurons increased progressively in the anterior preoptic area, suprachiasmatic area and infundibulum. FMRFamide-ir neurons were never revealed in mesencephalon and rhombencephalon. Numerous ir fibers terminated in the median eminence and intermediate lobe of the pituitary. The adult pattern of distribution of FMRFamide-ir elements in the brain was achieved during the postmetamorphic development. In light of the existing literature, the possible placodal origin of forebrain-located FMRFamide neurons is briefly discussed.

Animals↗
PubMed1976

Electrophysiological evidence for a topographical projection of the nasal mucosa onto the olfactory bulb of the frog.

Three olfactory nerve branches respectively subserving either a medial, an intermediate, or a lateral region of the dorsal olfactory receptor sheet of the bullfrog Rana catesbeiana were electrically stimulated with bipolar platinum hook electrodes. Extracellular single unit responses from 93 second-order cells in different regions of the olfactory bulb were recorded with metal-filled glass micropipets. The excitatory responsiveness of each unit to the stimulation of each of the three nerve branches (response profile) was determined. Some units were sensitive to stimulation of each of the three nerve branches, thus suggesting a wide projection from the entire receptor sheet. On the other hand, other units were more selective. Of this latter group, units in the lateral bulb were excited by nerve branches subserving the more lateral regions of the receptor sheet; units in the medial bulb were excited by the nerve branches subserving the more medial regions of the receptor sheet. These data provide electrophysiological evidence for a topographical projection of the olfactory receptor sheet onto the olfactory bulb, and further suggest that the projections onto different bulbar cells vary in degree of localization.

Animals↗
PubMed2005

Changes in glutamate receptor subunit 4 expression in the deafferented olfactory bulb of zebrafish.

The distribution of ionotropic glutamate receptor subunit 4 (iGluR4) was examined in both normal and deafferented olfactory bulbs of adult zebrafish, Danio rerio. With the exception of the olfactory nerve layer, there was extensive labeling with antibodies to iGluR4 in the olfactory bulbs, specifically in juxtaglomerular cell bodies and their processes. These results are consistent with previous work, which has suggested differential distribution of glutamate receptors in the vertebrate olfactory system. Analysis of bulbs following olfactory organ removal revealed a significant loss of iGluR4 immunoreactivity by 24 h post-deafferentation. At 48 h after denervation, iGluR4 labeling had returned to normal levels and was retained through 3 weeks post-surgery. Thus, afferent input plays a role in reduced labeling of this protein immediately following injury, but return of immunoreactivity can occur even without sensory innervation.

Animals↗
PubMed2001

Intranasal inoculation with the olfactory bulb line variant of mouse hepatitis virus causes extensive destruction of the olfactory bulb and accelerated turnover of neurons in the olfactory epithelium of mice.

Viral upper respiratory infections are the most common cause of clinical olfactory dysfunction, but the pathogenesis of dysosmia after viral infection is poorly understood. Biopsies of the olfactory mucosa in patients that complain of dysosmia after viral infection fall into two categories: one in which no olfactory epithelium is seen and another in which the epithelium is disordered and populated mainly by immature neurons. We have used intranasal inoculation with an olfactory bulb line variant of MHV to study the consequences of viral infection on peripheral olfactory structures. MHV OBLV has little direct effect on the olfactory epithelium, but causes extensive spongiotic degeneration and destruction of mitral cells and interneurons in the olfactory bulb such that the axonal projection from the bulb via the lateral olfactory tract is markedly reduced. Moreover, surviving mitral cells apparently remain disconnected from the sensory neuron input to the glomerular layer, judging from retrograde labeling studies using Dil. The damage to the bulb indirectly causes a persistent, long-term increase in the turnover of sensory neurons in the epithelium, i.e. the relative proportion of immature to mature sensory neurons and the rate of basal cell proliferation both increase. The changes that develop after inoculation with MHV OBLV closely resemble the disordering of the olfactory epithelium in some patient biopsies. Thus, damage to the olfactory nerve or bulb may contribute to a form of post-viral olfactory dysfunction and MHV OBLV is a useful model for studying the pathogenesis of this form of dysosmia.

Administration, Intranasal↗
PubMed1998

Viral replication in olfactory receptor neurons and entry into the olfactory bulb and brain.

This communication describes our ongoing studies of the interaction of the mouse host and vesicular stomatitis virus (VSV). When VSV is applied to the nasal neuroepithelium, it initially replicates in olfactory receptor neurons, and is transmitted along the olfactory nerve to the central nervous system (CNS) within 12 hours. In the olfactory bulb, the virus replicates invasively through the layers of the olfactory bulb, reaching the olfactory ventricle by day 4-5 post infection, and the hindbrain by day 8 post infection. In mice, infection may result in a 50% mortality rate. The crucial host innate and specific immune responses responsible for restricting viral propagation and caudal spread of the virus will be discussed. The efficacy of interleukin-12 (IL-12) treatment for enhanced viral clearance and promotion of host recovery are described along with the implications for treatment of human encephalitis. The hosts' response to infection is also regulated by the sex of the host, and the age at infection. The role of specific mucosal humoral immunity and systemic cellular immunity in prevention of infection are described.

Animals↗
PubMed2001

Mechanisms of axonal plasticity: lessons from the olfactory pathway.

The olfactory pathway has emerged recently as an effective model for studying general principles of axon extension and regeneration. A variety of both trophic as well as repulsive molecules are found in the olfactory pathway and are being characterized for their roles in promoting the high capacity for plasticity and growth in olfactory receptor cell axons. In addition, olfactory ensheathing cells, which line the olfactory nerve, have been shown to promote axon extension not only in the olfactory pathway but also in the injured spinal cord. This review summarizes some of our current knowledge of these mechanisms and how they may function collectively to promote axon plasticity.

Animals↗