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PubMed1984

An HRP study of neural pathways to neocortical olfactory areas in monkeys.

Afferent fiber projections to the two orbitofrontal olfactory areas of monkeys were studied using the horseradish peroxidase (HRP) technique. After injections of HRP into the lateroposterior (LPOF) or centroposterior (CPOF) area of the orbitofrontal cortex, some differences were found in the distribution of labeled cells between the projections to the LPOF and CPOF. These results, along with those of previous electrophysiological investigations, suggest the following conclusions: (1) the extrathalamic olfactory pathway to the LPOF identified by Tanabe et al. has relay neurons primarily in the substantia innominata and the amygdala and, secondarily, in the prorhinal cortex and the hypothalamus; (2) direct fibers to the LPOF from the amygdala and the prorhinal cortex pass through the areas ventral to the thalamus; (3) the transthalamic olfactory pathway to the CPOF identified by Yarita et al. has relay neurons concentrated primarily in the magnocellular portion of the mediodorsal nucleus of the thalamus.

Animals↗
PubMed1980

Autoradiography of the olfactory-hippocampal pathway in the cat with special reference to the perforant path.

The anatomical pathway from the prepyriform cortex to the hippocampus in the cat was traced autoradiographically by means of anterograde transport of [3H] leucine. A direct projection from the prepyriform cortex to the lateral entorhinal area was confirmed in the cat: the termination of these fibers was largely confined to the outer part of the molecular layer. From the lateral entorhinal area, the perforant path fibres terminate on the most distal parts of the dendrites of the hippocampal granule and pyramidal cells. However, differences between cat and rat were found with respect to the terminations in the CA1 area.

Animals↗
PubMed1986

Olfactory evoked potentials in the rat.

Routine clinical assessment of the integrity of the olfactory pathway using olfactory evoked potentials remains an elusive goal. One important difficulty arises from the uncertainty of the exact origin of the potentials: are they produced by olfactory or trigeminal elements? To resolve this problem, an animal model using the rat was developed. Amylacetate was used as an odorant stimulus, and potentials were measured and computer averaged after elimination of trigeminal and vomeronasal activity. A positive-negative wave was recorded from the olfactory bulb surface, and a negative wave often followed by a positive wave was recorded from the surface of the cerebral cortex. Measurements from the scalp surface gave comparable results. Lesioning experiments of the olfactory pathway indicate that the evoked potentials recorded at the vertex originate in the ventral forebrain, specifically in the prepyriform cortex, olfactory tubercle, and anterior olfactory nucleus.

Animals↗
PubMed2000

Expression of EphA5 during development of the olfactory nerve pathway in rat.

The olfactory neuroepithelium is a highly plastic region of the nervous system that undergoes continual turnover of primary olfactory neurons throughout life. The mechanisms responsible for persistent growth and guidance of primary olfactory axons along the olfactory nerve are unknown. In the present study, we used antibodies against the Eph-related receptor, EphA5, to localise EphA5, and recombinant EphA5-IgG fusion protein to localise its ligands. We found that although both EphA5 and its ligands were both expressed by primary olfactory neurons within the embryonic olfactory nerve pathway, there was no graded or complementary expression pattern. In contrast, the expression patterns altered postnatally such that primary olfactory neurons expressed the ligands, whereas the second-order olfactory neurons, the mitral cells, expressed EphA5. The role of EphA5 was analysed by blocking EphA5-ligand interactions in explant cultures of olfactory neuroepithelium using anti-EphA5 antibodies and recombinant EphA5. These perturbations reduced neurite outgrowth from explant cultures and suggest that intrafascicular axon repulsion may serve to limit adhesion and optimise conditions for axon growth.

Aging↗
PubMed1996

Evidence for different chemosensory signal transduction pathways in olfactory and vomeronasal neurons.

Both the olfactory and vomeronasal epithelia mediate chemosensory reception. Here we report that several molecules that are highly expressed in the olfactory epithelium and therefore are likely to be important mediators of olfactory signal transduction (Golfalpha, adenylyl cyclase III and the olfactory cyclic nucleotide gated ion channel) are not present in the vomeronasal epithelium. Therefore it appears that distinct molecules mediate chemosensory signal transduction in the olfactory and vomeronasal epithelia. The genes for Golfalpha, adenylyl cyclase III, the olfactory cyclic nucleotide gated ion channel, Ggamma8 and olfactory marker protein which are all expressed in the olfactory epithelium have consensus Olf-1 binding sites. The transcription factor Olf-1 was found to be highly expressed in the olfactory epithelium and was detected at a similar level in the vomeronasal epithelium. The expression pattern of Olf-1 did not correlate with that of molecules involved in olfactory signaling but was more similar to the expression pattern of Ggamma8 and olfactory marker protein which are found both in olfactory and vomeronasal neurons. Therefore, expression of Olf-1 in the olfactory epithelium and the presence of Olf-1 binding sites in a number of different genes found to be expressed in the olfactory epithelium are not sufficient to explain the observed gene expression patterns.

Adenylyl Cyclases↗
PubMed1999

Expression of galectin-1 in the olfactory nerve pathway of rat.

The olfactory neuroepithelium is characterised by the mosaic distribution of primary olfactory neurons that express different odorant receptors and cell surface glycoconjugates. Carbohydrates are believed to form a glycocode that mediates sorting out and fasciculation of primary olfactory axons through interactions with carbohydrate-binding proteins such as galectin-1. In the present study, we describe in detail the expression pattern of galectin-1 in the developing and adult rat olfactory system. We demonstrate that galectin-1 is expressed by olfactory ensheathing cells both in olfactory nerve and within the nerve fibre layer of the olfactory bulb of the embryonic and adult rat. In the adult rat, galectin-1 was preferentially expressed by olfactory ensheathing cells in the nerve fibre layer of the ventromedial and lateral surfaces of the olfactory bulb. Galectin-1 was also expressed by subsets of periglomerular cells and granule cells, particularly in the ventromedial region of the olfactory bulb. In adult rat, the galectin-1 ligand, N-acetyl-lactosamine, was expressed by primary olfactory axons that terminated in glomeruli present in the ventromedial and lateral olfactory bulb. These results suggest that expression of galectin-1 may provide a mechanism for the sorting of subpopulations of axons in the nerve fibre layer of the olfactory bulb during development as well as play a role in the postnatal maintenance of specific glomerular connections.

Aging↗
PubMed1996

Differential adhesion and the initial assembly of the mammalian olfactory nerve.

During the initial assembly of the olfactory pathway, the behavior of olfactory axons changes as they grow from the olfactory epithelium toward the telencephalic vesicle. The axons exit the epithelium singly or in small fascicles, and their growth cones are simple and bullet-shaped. Outside the epithelium, they make a sharp dorsal turn and fasciculate into a single nerve; the growth cones remain simple. Upon entering the ventromedial telencephalon, the axons defasciculate, branch extensively, and end in complex, lamellate growth cones which extend toward the ventrolateral aspect of the telencephalic vesicle. The distribution of laminin, collagen-IV, and fibronectin varies in register with these changes in olfactory axon and growth cone behavior. Each of these extracellular matrix molecules influences olfactory neurite outgrowth and growth cone morphology in vitro consistent with its distribution in vivo. The distribution of E-cadherin, L1, neural cell adhesion molecule (NCAM) and the polysialated form of NCAM also varies in register with changes in olfactory axon behavior. In vitro, L1 modulates embryonic olfactory neurite outgrowth and growth cone morphology consistent with its distribution in vivo. Thus, olfactory axon trajectory, fasciculation, and growth cone morphology change within distinct adhesive environments in the nascent olfactory pathway, and some of the molecules that characterize these environments have differential effects upon olfactory neurite growth and growth cone morphology. Consequently, the patterned expression and activity of extracellular matrix and cell surface adhesion molecules may contribute to the initial assembly of the olfactory pathway.

Animals↗
PubMed1996

Expression of extracellular matrix molecules and cell surface molecules in the olfactory nerve pathway during early development.

The spatial and temporal expression patterns of several extracellular matrix molecules--laminin and fibronectin and cell surface molecules, neural cell adhesion molecule (NCAM), L1, tenascin, chondroitin sulfate proteoglycan, and peanut agglutinin (PNA) binding sites--were investigated during early olfactory nerve development. NCAM and L1 have similar patterns: They are expressed in the olfactory nerve and on the olfactory receptor neurons (ORNs) commencing with the earliest olfactory axon outgrowth (E12-E15). Their expression patterns suggest that both NCAM and L1 are associated with extension and fasciculation of olfactory axons. A comparison of L1 and olfactory marker protein suggests that L1 is expressed predominantly on immature ORNs. Laminin has an unique punctate staining pattern in the developing olfactory pathway as early as E12. These laminin puncta might play a role in olfactory neurite outgrowth and guidance. At E14, when pioneer olfactory axons enter the brain, the laminin-positive meninges on the surface of the olfactory bulb primordium break down but remain intact in the rest of the telencephalon. This suggests a functional interaction between the olfactory axons and the glial-pial barrier. Fibronectin staining is diffuse throughout the cranial mesenchyme but is absent from the olfactory nerve pathway. No specific patterns of tenascin or chondroitin sulfate, were observed during early olfactory development. PNA binding sites were associated with olfactory axon fasciculation. The expression of several extracellular matrix molecules and cell surface molecules is spatially and temporally regulated in the developing olfactory system. These molecules, thus, may play functional roles in olfactory axon outgrowth, fasciculation, and/or guidance.

Animals↗
PubMedDate not supplied

Making scents of olfactory neurogenesis.

Olfaction was long considered to belong more to the realm of art than to that of science. As a result, how the brain perceives, discriminates, and recognizes odorant molecules is still a mystery. Recent progress has nonetheless been made at early stages of the olfactory pathway when olfactory studies entered into the molecular era to elucidate the first contact of an odor molecule with a receptor. Our group focuses on the analysis of odor information in the olfactory bulb, the first processing relay in the mammalian brain. Using this model, we are attempting to decipher the code for odorant information. Furthermore, the olfactory bulb also provides an attractive model to investigate neuronal proliferation, differentiation, migration, and neuronal death, processes involving an interplay between genetic and epigenetic influences. Finally, our goal is to explore the possible consequences of the olfactory bulb plasticity, in olfactory performance. For these purposes, we aim to combine morphological, electrophysiological and behavioral approaches to investigate: (1) how the olfactory bulb processes odor molecule information, (2) how neural precursors differentiate into olfactory bulb interneurons, (3) how these newly-generated neurons integrate into an operational neural network, (4) what role they play in the adult olfactory bulb, and (5) how are basic olfactory functions maintained in such a sensory system subjected to continuous renewal of a large percentage of its neuronal population. These questions should provide new fuel for the molecular and cellular bases of sensory perception and shed light onto cellular bases of learning and memory.

Animals↗
PubMed2004

Plasticity in the olfactory system: lessons for the neurobiology of memory.

We are rapidly advancing toward an understanding of the molecular events underlying odor transduction, mechanisms of spatiotemporal central odor processing, and neural correlates of olfactory perception and cognition. A thread running through each of these broad components that define olfaction appears to be their dynamic nature. How odors are processed, at both the behavioral and neural level, is heavily dependent on past experience, current environmental context, and internal state. The neural plasticity that allows this dynamic processing is expressed nearly ubiquitously in the olfactory pathway, from olfactory receptor neurons to the higher-order cortex, and includes mechanisms ranging from changes in membrane excitability to changes in synaptic efficacy to neurogenesis and apoptosis. This review will describe recent findings regarding plasticity in the mammalian olfactory system that are believed to have general relevance for understanding the neurobiology of memory.

Animals↗
PubMed1994

Role of gp63 and gIII of Aujeszky's disease virus in the invasion of the olfactory nervous pathway in neonatal pigs.

The purpose of this study was to examine in which way envelope glycoproteins gp63 and gIII of Aujeszky's disease virus (ADV) are involved in neuropathogenesis in pigs. The Ka strain of ADV and its single deleted mutants were examined with respect to invasion and spread in the olfactory nervous pathway after intranasal inoculation in neonatal pigs. The olfactory mucosa, olfactory bulb and lateral olfactory tract representing the 1st, 2nd and 3rd neuronal level of the olfactory pathway respectively, were examined for virus by isolation and for antigen by immunocytochemical localization. The Ka undeleted strain and its gIII deleted mutant invaded and spread to all the neuronal levels in a similar way. The gp63 deleted mutant invaded and spread in the olfactory mucosa similarly to the Ka parental strain but its replication and degree of spread were diminished in all the levels of the central nervous system (CNS). It is, therefore, concluded that gp63 is involved in the neurotropism of ADV, while gIII is not.

Animals↗
PubMed1998

Molecular development of the olfactory nerve pathway.

There are, at least, two major questions concerning the molecular development of the olfactory nerve pathway. First, what are the molecular cues responsible for guiding axons from the nasal cavity to the olfactory bulb? Second, what is the molecular basis of axon targeting to specific glomeruli once axons reach the olfactory bulb? Studies in the primary olfactory pathway have focused on the role of extracellular matrix and ensheathing cells in establishing an initial substrate for growth of pioneer axons between the periphery and brain. The primary axons also express a multitude of cell adhesion molecules that regulate fasciculation of axons and hence may play a role in fascicle formation in the olfactory nerve. Although the olfactory neuroepithelium principally consists of a morphologically homogeneous class of primary olfactory neurons, there are numerous subpopulations of olfactory neurons expressing chemically distinct phenotypes. In particular, numerous subpopulations have been characterized by expression of unique carbohydrate residues and olfactory receptor proteins. Some of these molecules have recently been implicated in axon guidance and targeting to specific glomeruli.

Animals↗
PubMed1994

Role of envelope glycoproteins gI, gp63 and gIII in the invasion and spread of Aujeszky's disease virus in the olfactory nervous pathway of the pig.

One-week-old pigs were infected intranasally with the Ka strain of Aujeszky's disease virus (ADV) or with mutants that were lacking the non-essential envelope glycoproteins gI, gp63 or gIII. The invasion and spread of these strains in the olfactory nervous pathway were examined by assessing virus levels and by localizing viral antigens in the olfactory mucosa representing the first neuronal level, in the olfactory bulb representing the second neuronal level and in the lateral olfactory gyrus, the rostral perforated substance and the piriform lobe, all representing the third neuronal level. The Ka parental strain invaded and spread up to the third neuronal level. The extent of invasion and spread of the gIII- mutant were similar to those of the parental strain. The gp63- mutant replicated normally in the olfactory mucosa, but its spread to all the other levels was limited as compared with that of the parental strain. The gI- mutant showed a defect in infection at all neuronal levels. These results indicate that, of the non-essential envelope glycoproteins, gI plays the major role in neural invasion and spread of ADV in its natural host. The pattern of invasion and spread of these mutants in the olfactory pathway of pigs was similar to that previously observed in the trigeminal pathway. The type of nervous pathway therefore appears not to influence the neuropathogenesis of ADV or mutants deleted in non-essential envelope glycoproteins in the pig.

Animals↗
PubMed2005

Retinoic acid regulates postnatal neurogenesis in the murine subventricular zone-olfactory bulb pathway.

Neurogenesis persists throughout life in the rodent subventricular zone (SVZ)-olfactory bulb pathway. The molecular regulation of this neurogenic circuit is poorly understood. Because the components for retinoid signaling are present in this pathway, we examined the influence of retinoic acid (RA) on postnatal SVZ-olfactory bulb neurogenesis. Using both SVZ neurosphere stem cell and parasagittal brain slice cultures derived from postnatal mouse, we found that RA exposure increased neurogenesis by enhancing the proliferation and neuronal differentiation of forebrain SVZ neuroblasts. The RA precursor retinol had a similar effect, which was reversed by treating cultures with the RA synthesis inhibitor disulfiram. Electroporation of dominant-negative retinoid receptors into the SVZ of slice cultures also blocked neuroblast migration to the olfactory bulb and altered the morphology of the progenitors. Moreover, the administration of disulfiram to neonatal mice decreased in vivo cell proliferation in the striatal SVZ. These results indicate that RA is a potent mitogen for SVZ neuroblasts and is required for their migration to the olfactory bulb. The regulation of multiple steps in the SVZ-olfactory bulb neurogenic pathway by RA suggests that manipulation of retinoid signaling is a potential therapeutic strategy to augment neurogenesis after brain injury.

Animals↗
PubMed1995

Dual second-messenger pathways in olfactory transduction.

Increasing evidence indicates that inositol phosphate as well as cyclic nucleotide signalling pathways mediate olfactory transduction. Both pathways can target multiple ion channel effectors, suggesting that olfactory receptor cells serve as more than simple selectivity filters and that they possibly represent the first stage of olfactory integration.

Animals↗
PubMed1998

[Studying the possibility of respiratory immunization against tick-borne encephalitis].

There are known 3 likely mechanisms of virus conveyance into the central nervous system (CNS). These include hematogenic penetration, spread along the peripheral nerves, and the olfactory pathway which begins from the infected olfactory neuroepithelial cells. The possibility of viral spread into CNS via the olfactory pathway was shown for the representatives of togaviruses, herpesviruses, coronaviruses, rhabdoviruses, and for some others. This study suggests that the olfactory pathway of viral conveyance into CNS may be blocked by specific mucosal antibodies in the nasal mucosa. The recombinant TK- variant of WR vaccinia strain with inserted genes coding structural and nonstructural proteins of TBE virus is accumulated in the branches of the respiratory tract only while the parenteral vaccinia strain is detected in the brain regions, spleen, respiratory tract, and in blood. The protective activity of recombinant strain and inactivated TBE vaccine after mice immunization by escarification or intranasally, or subcutaneously was comparatively studied. The findings indicate that intranasal immunization by recombinant strain is the most protective against intraperitoneal challenge by TBE virus. The mucosal and humoral immune response that was induced by intranasal immunization seems to provide the highest levels of protection, which was experimentally observed.

Administration, Intranasal↗
PubMed1985

Immunohistopathologic analysis of olfactory degeneration caused by ischemia.

The development of olfactory dysfunction caused by ischemia was studied in Mongolian gerbils. Mongolian gerbils frequently have an anomaly of the cerebral circulation and are susceptible to brain ischemia or infarction following ligation of a single common carotid artery. Ischemia was induced by unilateral common carotid artery ligation or temporary occlusion of both common carotid arteries, and the olfactory pathway was examined. In the olfactory pathway of the forebrain, ischemic changes were observed in the lateral olfactory tract, olfactory tubercle, olfactory ventricle, and anterior olfactory nucleus. The olfactory bulb was resistant to ischemia. Partial or complete degeneration of the ipsilateral olfactory neuroepithelium was observed in some gerbils that survived more than 14 days after the onset of ischemia. Immunohistopathologic analysis of the neuroepithelium for the olfactory marker protein revealed that functional damage of the olfactory neurons occurred in some gerbils within the first few days after the ischemic event.

Animals↗