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At least 775 records · Page 43Linked to original sources
PubMed1990

Immunochemical markers for the frog olfactory neuroepithelium.

Monoclonal antibodies (mAbs) were generated that react with the major cell types in the olfactory neuroepithelium of the frog, Rana catesbeiana. This pseudostratified epithelium consists of apical supporting cells, a middle layer of olfactory receptor neurons and a heterogeneous population of basal cells consisting of basal cells proper and globose basal cells. Both olfactory receptor neurons and globose basal cells were labelled by mAb 13-OE, which recognized the neural cell adhesion molecule NCAM. The identity of these NCAM positive cells was established by analysing regenerating olfactory epithelium and by a double-antibody labelling immunofluorescence technique. The olfactory nerve was lesioned, which induced the death of olfactory receptor neurons and the subsequent proliferation of basal cells. When the regenerating olfactory epithelium was analysed prior to the reconstitution of mature olfactory neurons, mAb 13-OE reacted specifically with globose basal cells and not the basal cells proper. Simultaneous labelling of normal olfactory epithelium with mAb 13-OE and polyclonal anti-keratin antibodies, the latter of which labels supporting cells and basal cells proper, revealed no double-labelled cells. These results further confirmed that NCAM was expressed by both globose basal cells and receptor neurons but not by other cell types within the epithelium. Additional cell types in the olfactory epithelium reacted with other new mAbs: 4-OE, 5-OE, 7-OE and 9-OE. Supporting cells were stained by mAb 4-OE. Olfactory receptor neurons and the entire population of basal cells were immunoreactive with mAb 7-OE. The cilia and knobs of receptor neurons were strongly immunoreactive with mAb 5-OE whereas mAb 9-OE selectively stained olfactory knobs and not the cilia on these chemosensory cells. These studies are a first step towards experimental approaches designed to elucidate the mechanisms underlying the unique proliferative properties of the olfactory neuroepithelium in frog.

Animals↗
PubMed1995

Calmodulin, calbindin-D28k, calretinin and neurocalcin in rat olfactory bulb during postnatal development.

Odorant stimulation of receptor cells results in a calcium influx that activates the transduction pathway. The olfactory neurons extend axons to the olfactory bulb where they synapse onto mitral cells. Ca(2+)-acceptors also may participate in subsequent processing of olfactory information. The present study describes the distribution of calmodulin, calretinin, calbindin-D28k and neurocalcin during rat main olfactory bulb development. From postnatal day 1 (P1) we observed in the olfactory nerve layer a thin external bundle containing calbindin and calretinin whereas calmodulin was present in a large internal bundle. In tufted cells, neurocalcin immunoreactivity was detected at P10 and increased until P20. In mitral cells calmodulin was intensively immunoreactive at P1 but decreased during development to disappear at adulthood whereas calretinin was weakly labelled at P1 but raised in intensity until P20. In granule cells calbindin-D28k and calretinin were detected from P1. Giant neurons were positive for both calretinin and calbindin-D28k from postnatal day 20.

Aging↗
PubMed1995

Neurons of the olfactory organ projecting to the caudal telencephalon and hypothalamus: a carbocyanine-dye labelling study in the brown trout (Teleostei).

The caudal extrabulbar projections and their neurons of origin in the trout were studied after carbocyanine-dye (DiI) labelling in either the olfactory organ or the caudal telencephalon. DiI application to the caudal telencephalon labelled bipolar neurons in the olfactory epithelium, where they were sparsely distributed throughout the olfactory lamellae. Labelled fibres ran scattered in the olfactory nerve without forming bundles. DiI application to the olfactory organ labelled extrabulbar projections to the ventral telencephalon, preoptic region and tuberal hypothalamus. These results confirm that primary sensory fibres running in the medial olfactory tract of trout have an olfactory origin.

Animals↗
PubMed2001

Basic fibroblast growth factor and fibroblast growth factor receptors in adult olfactory epithelium.

Basic fibroblast growth factor (FGF2) stimulates proliferation of the globose basal cells, the neuronal precursor in the olfactory epithelium. The present study investigates the expression of basic fibroblast growth factor and fibroblast growth factor receptors in the adult olfactory epithelium. FGF2 immunoreactivity was expressed widely in the olfactory epithelium, with the highest density of immunoreactivity in the supporting cells. In contrast, most cells in the epithelium expressed FGF2 mRNA. Fibroblast growth factor receptor-1 (FGFr1) immunoreactivity was densest in the basal cell and neuronal layers of the olfactory epithelium and on the apical surface of supporting cells. In the lamina propria FGF2 immunoreactivity and mRNA were densest in cells close to the olfactory nerve bundles. FGFr1 immunoreactivity was heaviest on the olfactory ensheathing cells. Using reverse transcriptase-polymerase chain reaction analysis, the olfactory epithelium was shown to express only three receptor splice variants, including one (FGFr1c) with which basic fibroblast growth factor has high affinity. Other receptor splice variants were present in the lamina propria. Taken together, these observations indicate endogenous sources of FGF2 within the olfactory epithelium and lamina propria and suggest autocrine and paracrine pathways via which FGF2 might regulate olfactory neurogenesis. The observation of only three receptor splice variants in the olfactory epithelium limits the members of the fibroblast growth factor family which could act in the olfactory epithelium. The widespread distribution of receptors suggests that fibroblast growth factors may have roles other than proliferation of globose basal cells.

Age Factors↗
PubMed2001

Bilateral olfactory deprivation reveals a selective noradrenergic regulatory input to the olfactory bulb.

Unilateral olfactory deprivation in the rat induces changes in the catecholaminergic system of the olfactory bulb. Nevertheless, evidence suggests that unilateral deprivation does not fully prevent stimulation of the deprived bulb. The present report analyses the response of the catecholaminergic system of the olfactory bulb in fully deprived rats obtained by bilateral naris occlusion. The complete deprivation produces more rapid and dramatic changes in both the intrinsic and extrinsic catecholaminergic systems of the olfactory bulb. Intrinsic responses involve a rapid decrease in dopamine-containing cells to about 25% of controls, correlated with a decreased Fos expression in juxtaglomerular cells of all olfactory glomeruli, with the only exception of those of the atypical glomeruli which maintain unaltered expression of both markers. In parallel with these events, there is a progressive increase in the density of extrinsic noradrenergic axons arising from neurons in the locus coeruleus, which shows, in parallel, a progressive increase in Fos expression. This model demonstrates plastic changes in the catecholaminergic system of the olfactory bulb forming a valid morphological substrate for lowering thresholds in the processing of olfactory information. In addition to this generalized response, there is another one, directed to a specific subset of olfactory glomeruli (atypical glomeruli) involved in the processing of odor pheromone-like cues related to behavioral responses, that could be responsible for keeping active this reduced and selected group of glomeruli carrying crucial olfactory information. These results indicate the existence of adaptive changes in the catecholaminergic system of the olfactory bulb as a response to the lack of afferent peripheral stimulation. These changes involve dopamine- and noradrenaline-immunoreactive elements, in a strategy presumably directed at maintaining to the highest possible level the ability to detect olfactory signals.

Afferent Pathways↗
PubMed2003

Uptake of cobalt from the nasal mucosa into the brain via olfactory pathways in rats.

In the olfactory epithelium the primary olfactory neurons are in contact with the environment in the nasal cavity and they are also connected to the olfactory bulbs of the brain. These neurons may therefore provide a pathway by which foreign materials may reach the brain. Inhalation of cobalt-containing dust or fumes occurs in several workplaces, which may result in high exposure of the nasal tissues. In the present study, we used autoradiography and gamma-spectrometry to examine the transport of cobalt in the olfactory system after intranasal administration of 57Co2+ in rats. The results showed an uptake of the metal in the olfactory mucosa and a transport to the olfactory bulbs of the brain. The metal accumulated in the olfactory nerve layer and the terminals of the primary olfactory neurons in the glomerular layer of the bulb. In addition, low levels of cobalt were seen to migrate into the interior of the bulbs and the anterior parts of the olfactory cortex, indicating that the metal is able to leave the terminals of the primary olfactory neurons. Occupational exposure to cobalt, which is a neurotoxic metal, occurs in several workplaces, e.g. the hard metal industry. Memory deficits have been observed among workers exposed to hard metal via inhalation, and it was considered that cobalt may be the neurotoxic component of the hard metal. We propose that inhaled hard metal (as a dust powder or in a mist form) is deposited in the nasal passages and that released cobalt, after uptake into the brain via the olfactory pathway, may cause neurotoxicity. We consider that the olfactory route of entry of cobalt into the brain may be important and should be taken into account when risk assessments are performed concerning occupational inhalation of this metal.

Administration, Intranasal↗
PubMed2002

[Objective test of smell with cognitive potentials].

BACKGROUND: An objective smelling test is indicated for a reliable assessment of olfactory disorders. Usually olfactory evoked potentials (OEP) are registered. But the technique of this measurement is complicated and the generation of the OEP depends on the respiration of the subject. Alternatively, the contingent negative variation (CNV) can be used in the diagnosis of anosmia and parosmia, requiring only a simple olfactory stimulator. SUBJECTS AND METHOD: OEP and CNV were derived from 25 adults with normal smelling and from 16 patients with anosmia after head injury. First, the "direct" CNV was registered when the subjects expected a tone following a smell stimulus after 1.5 s. Using two different odors in a random order, the tone only followed one of them, so the "selective" CNV was scored. RESULTS: In both tests a distinct CNV was found in 21 and 23 normal smelling subjects, respectively. OEPs were absent in 4.3 % of this control group. No patient with anosmia showed an OEP or a CNV. The amplitudes of the "selective" CNV are significantly higher than those of the "direct" CNV. No gender dependency was found. CONCLUSION: The results show that an objective olfactometry can be realized by registration of CNV. Contrary to the measurement of OEP which depend on the physical parameters of olfactory stimuli, CNV correlates well with the cognitive identification of odor.

Adult↗
PubMed2005

[Preservation of olfaction in bifrontal craniotomies for lesions of the anterior and middle cranial fossa].

OBJECTIVE: The preservation of the olfactory tract during bifrontal approach for lesions located in the frontal skull base and the supra- and parasellar region has not previously been investigated. METHODS: In our study 12 patients underwent surgery for various lesions via the basal subfrontal route. All patients were observed prospectively, olfaction testing was performed pre- and postoperatively by an independent otorhinolaryngologist. RESULTS: We obtained complete preservation of the olfactory tracts and normal postoperative olfaction in all 12 cases. CONCLUSION: The bifrontal approach allowed a bilateral, wide operative field with excellent orientation and views of important structures. The shortcoming of this method, damage of the olfactory tracts and postoperative anosmia can be overcome.

Adolescent↗
PubMed1995

Human olfactory receptor neurons contain OMP mRNA in their dendritic and axonal processes.

The cellular expression of olfactory marker protein (OMP) mRNA and protein was investigated in the olfactory mucosa of humans ranging in age from 26 weeks of gestation to 85 years using in situ hybridization and immunocytochemistry. OMP mRNA and protein were most abundant in the somas of olfactory receptor neurons (ORNs). The hybridization signal over the ORN somal layer was greater in older subjects than in younger ones, reflecting either a higher neuronal density or more OMP mRNA per cell. In contrast, it was significantly lower in subjects with Alzheimer's disease when compared with an age-matched control. Characteristics of older subjects were patchiness in the distribution of OMP-expressing ORNs and the occurrence of subepithelial invaginations containing OMP-positive neurons. In addition, a significant hybridization signal was detected in the apical olfactory epithelium containing the dendrites, dendritic knobs, and cilia of ORNS, and over olfactory nerve bundles in the lamina propria, indicating the occurrence of OMP mRNA in dendritic and axonal domains.

Adult↗
PubMed2006

An updated review of clinical olfaction.

PURPOSE OF REVIEW: Disorders of the sense of smell can result through hundreds of different processes, but most commonly occur from upper-respiratory-tract infections, trauma, and chronic rhinosinusitis. RECENT DEVELOPMENTS: Research in the basic science of olfaction has progressed rapidly with powerful new molecular discoveries; however, our ability to treat these disorders remains limited. In clinical olfaction we are just realizing the broader existence of the sensory dysfunction in our population. We are discovering associations between neurodegenerative disorders and smell function that may allow us to identify these disorders earlier in the disease process. We are also challenging our previous categorization schemes and realizing that many etiologies cross the traditional conductive and neuro-sensory divisions. SUMMARY: Currently, aside from the possible therapeutic potential of systemic steroids, we have no effective treatment for the most common causes of olfactory loss. Recent advances in the basic science of olfaction provides us with an opportunity to develop new and novel clinical studies in an attempt at improving the quality of life for many of these patients.

Brain Injuries↗
PubMed2005

Distribution of D2 dopamine receptor in the olfactory glomeruli of the rat olfactory bulb.

Dopamine plays key roles in the processing of the olfactory information that takes place in the olfactory glomeruli. Previous studies using autoradiography demonstrate that, at the glomerular level, these actions are mainly mediated via activation of D2 dopamine receptors. Moreover, it has been suggested that D2 receptors could be present in the olfactory nerve, where they might modulate the entrance of olfactory input into the brain. Nevertheless, the precise subcellular localization of D2 receptors in the glomerular neuropil has not been investigated. In this report, we show the subcellular distribution of D2 receptors in the glomerular circuits of Wistar rats, using pre-embedding immunogold-silver labelling and electron microscopy. Present results demonstrate for the first time the presence of D2 dopamine receptors into the terminals of the olfactory axons. In addition, we demonstrate that D2 receptors are located into presynaptic elements of the glomerular neuropil other than the olfactory axons. These elements include the dendrites of the mitral/tufted cells and the dendrites of a subset of periglomerular cells that are GABAergic and dopaminergic. This distribution pattern provides anatomical support for a wide range of actions of dopamine in the glomerular circuits through presynaptic mechanisms mediated by D2 receptors. These actions would include: (i) modulation of the glutamate release from the olfactory axons to the dendrites of mitral/tufted cells and periglomerular cells; (ii) modulation of glutamatergic synapses from the dendrites of mitral/tufted cells to the dendrites of periglomerular cells and (iii) modulation of the neurotransmission from a subset of GABAergic/dopaminergic periglomerular cells to mitral/tufted cells.

Animals↗
PubMedDate not supplied

Olfactory neuroepithelioma arising from the olfactory placode.

The patient was a 54-year-old man, who had lost his sense of smell 6 years previously and had started to become forgetful about 6 months prior to presenting at hospital. MRI admission showed a large multicystic tumor with Gd-DTPA enhancement extending from the anterior cranial fossa through the sphenoid sinus and into the nasal cavity. Histopathological examination revealed extensive proliferation of small round cells that were divided by connective tissue septae. The tumor cells occasionally formed tubular structures, although no basement membranes were present. On immunostaining, round tumor cells were positive for neuron-specific enolase, synaptophysin, and chromogranin A, while cells forming tubules were positive for AE 1 and CAM 5.2. Almost all of the tumor cells were positive for Ber-EP4, and some of the epithelioid cells surrounding the tubular structures were also positive for luteinizing hormone-releasing hormone (LH-RH). Electron microscopy demonstrated sporadic intercellular junctions, many microtubules in the tumor cell processes, and clear- and dense-cored vesicles in the cytoplasm. Based on the results, this case appears to be the first documented neuroepithelioma with Ber-EP4- and LH-RH-positive cells arising from the olfactory placode.

Biomarkers, Tumor↗
PubMed1986

Quantitative autoradiographic localization of the D1 and D2 subtypes of dopamine receptors in rat brain.

The distribution of D1 and D2 receptors was studied in coronal sections of rat brain, using quantitative autoradiography. D1 receptors were labeled with 1.8 nM 3H-SKF-83566 (a brominated analog of 3H-SCH-23390), while D2 receptors were labeled with 1.0 nM 3H-spiroperidol (3H-SPD). The binding of both ligands to sections from brain and from a homogenate of caudate putamen (CPu mash) reached equilibrium within 80 min at 37 degrees C. CPu mash provided a virtually unlimited number of homogeneous sections that contained a high density of both D1 and D2 receptors. Sections of CPu mash were used in competition studies that confirmed that the specific binding of 3H-SKF-83566 was selective for D1 receptors, and that the binding of 3H-SPD was selective for D2 receptors. Scatchard analysis of equilibrium binding of the 2 ligands in the CPu in horizontal sections of rat brain revealed Kd values of 1.1 +/- 0.07 nM for 3H-SKF-83566 and 0.7 +/- 0.09 nM for 3H-SPD. Studies of the distribution of D1 and D2 receptors were carried out in coronal sections of brains from 5 rats. D1 receptors were found throughout the forebrain and were present in greater density than were D2 receptors in all regions examined except the olfactory nerve layer. In the CPu, nucleus accumbens, and olfactory tubercle, the densities of D1 and D2 receptors were, respectively, approximately 2,500 and 600-800 fmol/mg protein. In the substantia nigra, the density of D1 receptors was approximately 2,500 fmol/mg protein in both the compacta and the reticulata, but the density of D2 receptors was 230 fmol/mg protein in the compacta and 70 fmol/mg protein in the reticulata. The ventral tegmental area contained only 90 fmol/mg protein of D1 receptors, and D2 receptors were undetectable. The entopeduncular nucleus, zona incerta, and region of the ventral internal capsule had densities of D1 receptors of 550-950 fmol/mg protein and D2 receptor densities of less than 100 fmol/mg protein. Densities of D1 and D2 receptors were, respectively, 2,700 and 900 fmol/mg protein in the choroid plexus. Knowledge of the differences in the relative distributions of D1 and D2 receptors in various brain regions may increase our understanding of the functions of brain dopaminergic systems and may aid in the development of new therapeutic approaches for neuropsychiatric disorders.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗