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PubMed1998

A transient population of neurons pioneers the olfactory pathway in the zebrafish.

Mechanisms guiding the first axons from the olfactory placode of the peripheral nervous system (PNS) to the olfactory bulb in the vertebrate CNS are unknown. We analyzed the initial outgrowth of axons from the olfactory placode in zebrafish and found a precocious transient class of pioneer neurons that prefigure the primary olfactory pathway before outgrowth of olfactory sensory axons or expression of olfactory receptor genes. Not only are the pioneers antigenically, morphologically, and spatially distinct from olfactory sensory neurons, they are also developmentally distinct; via fate mapping, we show that they arise from a more anterior region of the lateral neural plate than do the first sensory neurons. After the axons of the sensory neurons grow into the CNS, the pioneer neurons undergo apoptotic cell death. When we ablated the pioneers before axonogenesis, the following sensory axons showed severe misrouting. We propose that the pioneers provide the first necessary connection from the PNS to the CNS and that they establish an axonal scaffold for the later-arriving olfactory sensory neurons.

Animals↗
PubMed1982

The role of the medial olfactory pathways in olfaction: behavioral and electrophysiological data.

The role of the olfactory inputs transmitted by the medial olfactory pathways --i.e. anterior limb of the anterior commissure and medial forebrain bundle-was studied in rats submitted either to a bilateral lesion of the anterior commissure (bAC group) or to a bilateral transection of the lateral olfactory tract followed by an anterior commissure bilateral lesion (bCL group). In the bCL group, the characteristic emotional reactions usually observed in sham-operated rats to biologically meaningful odorants (odor of a predator or of conspecifics) were no longer observed; in this group, the modulation of mitral cell electrical responses according to the biological meaning of the stimuli disappeared and no habituation was noted when the stimulations were repeated: few responses appeared at random; lastly, all the stimuli tested, the odor of conspecifics excepted, did not exert an awaking influence on the sleeping rats (slow wave sleep). On the contrary, emotional reactions were always observed in the bAC group, a slight increase of reactivity to the odorants was even noted. In this group of animals, the anterior commissure bilateral lesion induced a large increase of the bulbar responses to all the odorants; the habituation of the electrical responses disappeared, a large percentage of responses being always noted even for the tenth series of stimulation; these results point out the great inhibitory influence that the anterior commissure exerts on the olfactory bulb activity. In these bAC rats almost usual awaking influences were noted, however, the odor of conspecifics became as efficient as fox odor to awake the animals. Results are discussed in relation to the functional role of the medial and lateral olfactory pathways, the integrity of both the pathways being necessary for an accurate olfactory process.

Animals↗
PubMed2006

Once and again: retinoic acid signaling in the developing and regenerating olfactory pathway.

Retinoic acid (RA), a member of the steroid/thyroid superfamily of signaling molecules, is an essential regulator of morphogenesis, differentiation, and regeneration in the mammalian olfactory pathway. RA-mediated teratogenesis dramatically alters olfactory pathway development, presumably by disrupting retinoid-mediated inductive signaling that influences initial olfactory epithelium (OE) and bulb (OB) morphogenesis. Subsequently, RA modulates the genesis, growth, or stability of subsets of OE cells and OB interneurons. RA receptors, cofactors, and synthetic enzymes are expressed in the OE, OB, and anterior subventricular zone (SVZ), the site of neural precursors that generate new OB interneurons throughout adulthood. Their expression apparently accommodates RA signaling in OE cells, OB interneurons, and slowly dividing SVZ neural precursors. Deficiency of vitamin A, the dietary metabolic RA precursor, leads to cytological changes in the OE, as well as olfactory sensory deficits. Vitamin A therapy in animals with olfactory system damage can accelerate functional recovery. RA-related pathology as well as its potential therapeutic activity may reflect endogenous retinoid regulation of neuronal differentiation, stability, or regeneration in the olfactory pathway from embryogenesis through adulthood. These influences may be in register with retinoid effects on immune responses, metabolism, and modulation of food intake.

Animals↗
PubMed2002

The minimum number of neurons in the central olfactory pathway in relation to its function: a retrograde fiber tracing study.

The present study was aimed at determining the functionally essential size of the neuronal population in the central olfactory nervous system. Using conditioned rats who had learnt to avoid repellent (cycloheximide) solution by olfaction, varying degrees of injuries were made to the lateral olfactory tract, a major central olfactory pathway connecting the olfactory bulb to the olfactory cortex. After examining their olfactory ability to discriminate cycloheximide solution from water, intact bulbar projection neurons (mitral cells) with fiber connections to the olfactory cortex were quantified using a retrograde fiber tracing technique. The numbers of retrogradely labeled mitral cells from the rats with normal olfaction ranged between 20 and 92% of the control value, while those numbers from the anosmic rats ranged between 0 and 22%. We conclude that the functionally essential neuronal population is approximately one-fifth of the total in the central olfactory pathway, a presumed threshold value in terms of the ability to avoid cycloheximide solution by olfactory discrimination.

Animals↗
PubMed1996

Uptake of manganese and cadmium from the nasal mucosa into the central nervous system via olfactory pathways in rats.

In the olfactory epithelium the primary olfactory neurones are in contact with the environment and via the axonal projections they are also connected to the olfactory bulbs of the brain. Therefore, the primary olfactory neurones provide a pathway by which foreign materials may gain access to the brain. In the present study we used autoradiography and gamma spectrometry to show that intranasal instillation of manganese (54Mn2+) in rats results in initial uptake of the metal in the olfactory bulbs. The metal was then seen to migrate via secondary and tertiary olfactory pathways and via further connections into most parts of the brain and also to the spinal cord. Intranasal instillation of cadmium (109Cd2+) resulted in uptake of the metal in the anterior parts of the olfactory bulbs but not in other areas of the brain. This indicates that this metal is unable to pass the synapses between the primary and secondary olfactory neurones in the bulbs. Intraperitoneal administration of 54Mn2+ or 109Cd2+ showed low uptake of the metals in the olfactory bulbs, an uptake not different from the rest of the brain. Manganese is a neurotoxic metal which in man can induce an extrapyramidal motor system dysfunction associated with occupational inhalation of manganese-containing dusts or fumes. We propose that the neurotoxicity of inhaled manganese is related to an uptake of the metal into the brain via the olfactory pathways. In this way manganese can circumvent the blood-brain barrier and gain direct access to the central nervous system.

Administration, Intranasal↗
PubMed1998

Neurogenesis in the central olfactory pathway of adult decapod crustaceans.

Based on the previous findings that the number of olfactory projection neurons increases continuously in adult shore crabs, Carcinus maenas, and that this increase is associated with the presence of 5-bromo-2-deoxyuridine (BrdU)-positive, proliferating cells in the appropriate soma clusters (lateral soma clusters), we studied the further fate of these proliferating cells and the presence of apparent adult neurogenesis throughout the central olfactory pathway of diverse species of decapod crustaceans. Double labeling experiments combining biocytin-backfills and in vivo BrdU labeling as well as BrdU labeling with extended survival times (1 month) indicate that the cells proliferating in the lateral soma clusters of adult Carcinus undergo neuronal differentiation in about 3-4 weeks. In vivo BrdU labeling of different species representing important taxa of decapod crustaceans (shrimps, spiny lobsters, clawed lobsters, crayfish) revealed that neurogenesis among olfactory projection neurons is a constitutive feature of the adult decapod brain. In contrast, adult neurogenesis of the other neuron types present in the central olfactory pathway occurs in a taxon-specific manner and appears to be related to the development and reduction of accessory lobes throughout decapod phylogeny.

Animals↗
PubMed2003

Structural and functional changes in the olfactory pathway of adult Drosophila take place at a critical age.

The olfactory system of several holometabolous insect species undergoes anatomical changes after eclosion of the imago, following those occurring during metamorphosis. In parallel, odor experience and learning performance also evolve with age. Here, we analyze the case of adult Drosophila females. Synaptogenesis in the antennal lobe (AL) starts in late pupa and continues during the first days of adult life, at the same time as the behavioral response to odors matures. Individual olfactory glomeruli (DM6, DM2, and V) display specific growth patterns between days 1 and 12 of adult life. Experience can modify the olfactory pathway both structurally and functionally as shown by adaptation experiments. The modifications associated with this form of nonassociative learning seem to take place at a critical age. Exposure to benzaldehyde at days 2-5 of adult life, but not at 8-11, causes behavioral adaptation as well as structural changes in DM2 and V glomeruli. Altered levels in intracellular cAMP, caused by dunce and rutabaga mutants, do not affect the normal changes in glomerular size, at least at day 6 of development, but they prevent those elicited by experience, establishing a molecular difference between glomerular changes of intrinsic versus environmental origin. Taken together, these data demonstrate an imprinting-like phenomenon in the olfactory pathway of young Drosophila adults, and illustrate its glomerulus-specific dynamics.

Adaptation, Physiological↗
PubMed1999

Functional coupling in rat central olfactory pathways: a coherence analysis.

This experiment determined the importance of functional coupling between structures of central olfactory pathways: the olfactory bulb (OB), anterior (APC), posterior (PPC) parts of the piriform cortex and lateral entorhinal cortex (EC). From local field potential signals obtained in awake rats, coupling during spontaneous activity was estimated with variables reflecting level of coherence computed with a dynamical method. Results revealed a clear hierarchy in the strength of coupling between structures with dissociation within the piriform cortex: PPC was more tightly coupled with the EC than with APC. Systemic injection of a cholinergic antagonist, scopolamine, suggested that tonic coupling is strongly mediated by cortico-cortical connections and not by an external synchronizer, except between OB and APC.

Action Potentials↗
PubMed2000

Neurotrophic factors in the primary olfactory pathway.

The number of identified growth factors continues to increase rapidly with many being implicated in the development of the nervous system, although for most of them the autocrine and paracrine pathways of cellular regulation still remain to be elucidated. The primary olfactory pathway, consisting of the olfactory epithelium and olfactory bulb, is presented here as a very useful model for the analysis of growth factor function. Review of the available literature suggests that a large proportion of neuroactive growth factors and their receptors are present in the olfactory epithelium or olfactory bulb. Furthermore, the primary olfactory pathway is one of the most plastic in the nervous system with neurogenesis continuing to contribute new sensory neurones in the olfactory epithelium and new interneurones in the olfactory bulb throughout adult life. The rich diversity of growth factors and their receptors in the olfactory system indicates that it will be useful in elucidating how these molecules regulate the formation of the nervous system. The olfactory epithelium in particular is proving useful as a model for the actions of growth factors in directing the neuronal lineage from stem cell to mature neurone.

Animals↗
PubMed1991

Contributions of topography and parallel processing to odor coding in the vertebrate olfactory pathway.

Odor information appears to be encoded by activity distributed across many neurons at each level in the olfactory pathway. Thus olfactory circuits function as parallel distributed processors. New methods for observing distributed activity in such systems permit computer simulations to be constructed that are constrained by patterns of activity observed in the real system. Analysis of the system using a combination of physiological measurements and computational approaches might elucidate the principles by which odors are discriminated.

Animals↗
PubMed1980

A transthalamic olfactory pathway to orbitofrontal cortex in the monkey.

1. Evoked potentials restricted to the magnocellular portion of the mediodorsal nucleus (MDmc) of the thalamus were recorded after stimulation of the olfactory bulb (OB) and the posterior orbital cortex of the frontal lobe (OFC). Potentials evoked by stimulation of OB were probably trans-synaptically elicited, while potentials evoked by stimulation of OFC were probably a result of antidromic activation. 2. The area in which stimulation could elicit antidromic evoked potentials in MDmc was located in the centroposterior portion of OFC (CPOF). This area corresponds approximately to Walker's (80) area 13 and to von Bonin and Bailey's (9) area FF, and is situated medial and just anterior to a previously identified olfactory area, the lateroposterior portion of OFC (LPOF), which receives olfactory impulses through the hypothalamus. 3. Using extracellular microelectrodes, 58 neurons that responded with short latencies to OFC stimulation were identified in MDmc. To determine whether these neurons were activated antidromically by CPOF stimulation, three conventional neurophysiological criteria were applied; 20 of 58 neurons satisfied all the three criteria. Hence, they were concluded to be thalamocortical relay (TCR) neurons. 4. Intracellular recording of MDmc neurons disclosed that CPOF stimulation elicits an antidromic spike potential accompanied by an afterhyperpolarization. This hyperpolarization was presumed to be due to concurrent stimulation of inhibitory orbitothalamic fibers. It was also shown that EPSP-like depolarizations with superimposed spike potentials often occurred in the middle of the afterhyperpolarization. 5. Intracellular recording of MDmc neurons strongly suggested that the remaining 38 neurons that did not satisfy one of the three criteria were also TCR neurons. 6. These studies provide electrophysiological evidence for a transthalamic olfactory pathway from OB through MDmc to CPOF. 7. Using an extracellular recording technique, responses of neurons to eight odors were examined in CPOF and MDmc of unanesthetized awake monkeys. When these results were compared with the responses of neurons to the same odors in OB, prepyriform-amygdaloid area, and LPOF, it was concluded that the newly found transthalamic olfactory pathway to CPOF is very different in function from the previously demonstrated transhypothalamic olfactory pathway to LPOF.

Animals↗
PubMed2005

Noses and neurons: induction, morphogenesis, and neuronal differentiation in the peripheral olfactory pathway.

Non-axial mesenchymal/epithelial (M/E) induction guides peripheral olfactory pathway differentiation using cellular and molecular mechanisms similar to those in the developing limbs, aortic arches, and branchial arches. At each of these bilaterally symmetric sites off the midline axis, a thickened ectodermal epithelium is apposed to a specialized mesenchyme derived largely, but not exclusively, from the neural crest. The capacity of M/E interaction in the olfactory primordia (the combined olfactory placodal epithelium and adjacent mesenchyme) to induce a distinct class of sensory receptor neurons-olfactory receptor neurons-suggests that this mechanism has been modified to accommodate neurogenesis, neurite outgrowth, and axon guidance, in addition to musculoskeletal differentiation, chondrogenesis, and vasculogenesis. Accordingly, although the olfactory primordia share signaling molecules and transcriptional regulators with other bilaterally symmetric, non-axial sites such as limb buds, their activity may be adapted to mediate distinct aspects of cellular differentiation and process outgrowth during the initial assembly of a sensory pathway-the primary olfactory pathway-during early forebrain development.

Animals↗
PubMed1998

The expression of tenascin-C along the lamprey olfactory pathway during embryonic development and following axotomy-induced replacement of the olfactory receptor neurons.

Extracellular guidance molecules affect the pathway of growing axons by both attractive and repulsive interactions. Tenascin-C, a glycoprotein of the extracellular matrix, is localized along developing axonal pathways where it may function by repulsion, restricting axons within specific boundaries. The lamprey olfactory pathway offers an advantageous model for studying the role of extracellular matrix proteins in axon guidance because the entire pathway is readily seen in horizontal sections and because lesioning the olfactory nerve will induce the system into a new phase of coordinated neurogenesis and axon outgrowth. Although tenascin-C expression was absent during embryonic development, olfactory nerve fascicles contained tenascin-C-immunoreactivity (IR) during the larval stage. During retrograde degeneration, the fascicles lost tenascin-C-IR. Diffuse unfasciculated axonal processes extending from the olfactory epithelium did not express tenascin-C-IR; however, acetylated tubulin and GAP-43-IR was present, indicating axonal outgrowth. When the newly extended axons of olfactory receptor neurons converged to form fascicles, tenascin-C-IR was evident within the fascicular boundaries. The absence of tenascin-C expression when axonal process were short and diffuse, and its return when axons coalesced within fascicles, supports the view that tenascin-C functions as a boundary molecule in the olfactory pathway.

Animals↗
PubMed1991

Immunohistological demonstration of spread of Aujeszky's disease virus via the olfactory pathway in HPCD pigs.

The spread of Aujeszky's disease virus (ADV) from nasal mucosa via the olfactory pathway was studied in HPCD pigs. ADV antigen was detected in the epithelial cells, nasal gland cells, olfactory nerve cells and peripheral nerve fibres in the nasal cavity and in neuroglial cells in the olfactory bulb. Results indicate that the olfactory pathway is one of the most important neuronal pathways of ADV infection in pigs.

Animals↗
PubMed1998

Uptake of inorganic mercury in the olfactory bulbs via olfactory pathways in rats.

Uptake and transport in the olfactory neurons may be an important means by which some heavy metals gain access to the brain. In the present study we explored whether inorganic mercury (203Hg2+) may be taken up in the CNS via the olfactory pathway. Autoradiography and gamma spectrometry showed that intranasal instillation of 203Hg2+ in the right nostrils of rats resulted in much higher levels of the metal in the right olfactory bulbs than in the left ones. At the side of the application of the 203Hg2+ there was also a labeling of the olfactory nerve bundles projecting to the olfactory bulbs as well as in the olfactory nerve-fibres constituting the olfactory nerve layer of the bulbs, which was not seen on the opposite side. The results also showed that the 203Hg2+ accumulated in the glomerular layer of the bulbs. These data indicate that our results can be ascribed to a movement of the mercury along the olfactory axons to their terminal parts in the glomeruli and not to circulatory uptake from the mucosal vasculature. At late survival intervals a low labeling was also discernable in the external plexiform layer, indicating that a low level of 203Hg2+ leaves the terminal arborizations of the axons in the glomeruli. An uptake of 203Hg2+ in the glomerular layer of the olfactory bulbs was also seen in rats given the metal intraperitoneally. This uptake was similar in the right and left bulbs and always much lower than in the right bulbs of the rats given 203Hg2+ in the right nostrils. The intraperitoneal injections in addition resulted in an uptake of the 203Hg2+ in the olfactory epithelium. We propose that in these rats the mercury is taken up from the blood into the olfactory neurons and then moves along the axons to their terminations in the olfactory bulbs. In humans a continuous exposure of the nasal cavity to mercury vapor (Hg0), released from amalgam fillings and oxidized to Hg2+ in the olfactory mucosa, as well as a potential uptake of Hg2+ in the olfactory neurons from the blood, may lead to considerable concentrations of the metal in the olfactory bulbs.

Animals↗
PubMed1999

Development of a glia-rich axon-sorting zone in the olfactory pathway of the moth Manduca sexta.

Olfactory receptor cells (ORCs) of a particular odor tuning are dispersed in the olfactory epithelium, but their axons converge on distinct glomeruli in primary olfactory centers. As a consequence, axon associations must change to bring axons of ORCs with the same odor specificity together. Studies in Manduca sexta have indicated that just before they enter the antennal lobe (AL), ORC axons undergo extreme reorganization, finally entering the AL in fascicles destined for subsets of glomeruli. This axon-sorting zone is heavily populated by glial cells, and ORC axon growth cones often are in close physical contact with the glia. In moths rendered glia deficient, ORC axons fail to fasciculate in this region. Using propidium iodide to label nuclei and 5-bromo-2'-deoxyuridine to monitor proliferation, we found that the glia in the sorting zone arise from the AL, appearing shortly after the first ORC axons arrive. Experimental removal of some or all of the sensory innervation revealed that proliferation of sorting-zone glia is triggered by ORC axons. A second set of glia arises in the antenna and migrates along the antennal nerve toward the brain, populating the nerve after the establishment of the sorting zone. Development of this type of glial cell is independent of contact of the ORC axons with their central targets. We conclude that the sorting zone arises from CNS glia in response to ingrowth of ORC axons, and a critical number of glia must be present in the sorting zone for axons to correctly establish new neighbor-neighbor associations.

Aging↗
PubMed1998

Cellular and molecular neuropathology of the olfactory epithelium and central olfactory pathways in Alzheimer's disease and schizophrenia.

Specific deficits in odor detection threshold, identification, and memory have been recognized in a variety of disorders including the neurodegenerative disorder, Alzheimer's disease (AD), and the psychiatric illness, schizophrenia, which is likely due to abnormalities in neurodevelopment. Neuropathological abnormalities in peripheral and central olfactory systems have been described in both disorder. In the olfactory, epithelium, dystrophic neurites that are immunoreactive for tau, neurofilaments and other polypeptides, as well as deposits of beta-amyloid have been observed, and these findings have been thought to contribute to the olfactory dysfunction of these disorders. However, similar findings also occur in the olfactory epithelium of many normal individuals and those with various other neurodegenerative diseases. In contrast, neuropathological studies have reported selective vulnerability of central olfactory pathways for the accumulation of neurofibrillary pathology in AD, and for cytoarchitectural, neuronal morphometric, and cytoskeletal protein abnormalities suggestive of abnormal neurodevelopment in schizophrenia. Thus, it is likely that the olfactory impairments associated with these diseases are due to damage within central olfactory pathways, and that they are further amplified by the less specific impairments associated with age-related sensory neuroepithelial abnormalities. Finally, both the olfactory epithelium and central olfactory pathways represent model systems in which to study the neurobiology of these disorders, which ultimately may yield clues with diagnostic and therapeutic utility.

Alzheimer Disease↗
PubMed1985

Olfactory marker protein in the human olfactory pathway.

The presence of olfactory marker protein (OMP) in the olfactory tissue of rats, gerbils, and humans was demonstrated with goat antiserum to rat OMP. In control studies on rat neural tissue, OMP was found to be located in the olfactory receptor cells, nerves, and bulbs. Likewise, staining of OMP was found in the olfactory tissues of gerbils. Olfactory marker protein reactivity was also demonstrated in human olfactory receptor cells, nerves, and bulbs. The reactivity of OMP in human olfactory neurons to goat antiserum has allowed determination of the exact junction of olfactory and respiratory epithelia immunohistochemically.

Aged↗