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At least 19 recordsLinked to original sources
PubMed1996

Cell surface-associated extracellular distribution of a neural proteoglycan, 6B4 proteoglycan/phosphacan, in the olfactory epithelium, olfactory nerve, and cells migrating along the olfactory nerve in chick embryos.

The immunocytochemical and immuno-electron microscopic distribution of a neural proteoglycan (PG) was investigated with a monoclonal antibody, MAb 6B4, in the olfactory epithelium, the olfactory nerve, and the cells originating the epithelium and migrating along the olfactory nerve toward the forebrain in chick embryos. The PG recognized by MAb 6B4, that is 6B4 PG, in the brain of early postnatal rats, is identical to phosphacan. In chick embryos, immunoreactivity to 6B4 PG appeared on embryonic day (ED) 3-3.5 in a thin layer beneath the olfactory epithelium. It disappeared immediately, then becoming apparent in the bundles of the olfactory nerve. The immunoreactivity in the nerve bundles gradually increased during ED 5-11. On the other hand, cell surface-associated extracellular localization of the immunoreactivity was seen in the olfactory epithelium on ED 6 and afterwards. Immunofluorescent double-labeling of 6B4 PG and gonadotropin-releasing hormone (GnRH) revealed that the cell bodies of both GnRH-containing cells and other cells migrating along the olfactory nerve were surrounded by a rim immunoreactive to the PG. Under an electron microscope, the surfaces of the cell bodies and of the neurites in the nerve bundles were surrounded by deposits immunoreactive to 6B4 PG. These results indicate that 6B4 PG in chick embryos is one type of cell surface-associated extracellular matrix molecule, and that 6B4 PG covered the surfaces of migrating cells and of elongating olfactory nerve. The cell surface-associated extracellular localization of 6B4 PG found in the nasal region, taken together with the binding properties of this PG with cell adhesion molecules shown in rat brains, suggested that 6B4 PG played a role in guiding the migration of cells along the olfactory nerve in chick embryos.

Animals↗
PubMed2001

Volumetric and horseradish peroxidase tracing analysis of rat olfactory bulb following reversible olfactory nerve lesions.

Olfactory receptor neurons can regenerate from basal stem cells. Receptor neuron lesion causes degenerative changes in the olfactory bulb followed by regeneration as new olfactory receptor axons innervate the olfactory bulb. To our knowledge, parametric analyses of morphometric changes in the olfactory bulb during degeneration and regeneration do not exist except in abstract form. To better characterize olfactory bulb response, we performed morphometric analysis in rats following reversible olfactory nerve lesion with diethyldithiocarbamate. We also performed anterograde tracing of the olfactory nerve with wheatgerm agglutinin linked to horseradish peroxidase. Results of morphometry and tracing were complementary. The glomerular layer and external plexiform layer showed shrinkage of 45 and 26%, respectively, at 9 days. No significant shrinkage occurred in any other layer. Individual glomeruli shrank by 40-50% at 3 and 9 days following lesion. These data show that degenerative changes occur both in the glomeruli and transneuronally in the external plexiform layer. Olfactory nerve regeneration (identified by WGA-HRP transport) paralleled volumetric recovery. Recovery occurred first in ventral and lateral glomeruli between 9 and 16 days followed by recovery in medial and dorsal glomeruli. These data indicate substantial transynaptic degeneration in the olfactory bulb and a heretofore unrecognized gradient in olfactory nerve regeneration that can be used to systematically study recovery of a cortical structure.

Animals↗
PubMed2005

Olfactory ensheathing cells and olfactory nerve fibroblasts maintain continuous open channels for regrowth of olfactory nerve fibres.

The ensheathing cells of the olfactory nerves are arranged end-to-end to form a continuous channel enclosing the olfactory axons from their origin in the olfactory mucosa to their termination in the olfactory bulb. On their outer surface, the olfactory ensheathing cell channels have a basal lamina and an outer encirclement of olfactory nerve fibroblasts. We present an anatomical model of the ensheathing arrangements for the entire transit of the olfactory axons from the horizontal basal cells of the mucosa through the nerves to the superficial astrocytes of the bulb. We used intracranial section of the olfactory nerves to induce a rapid retrograde loss of olfactory neurons and degeneration of their axons, followed by replacement of the neurons from stem cells in the mucosa and growth of the newly formed axons along the olfactory nerves. The olfactory ensheathing cells survive and play a vital role in this process. Unlike Schwann cells in damaged peripheral nerve, the olfactory ensheathing cells neither divide nor migrate. They are actively phagocytic for removal of the degenerating axons, and provide continuous stable open channels along which adventitious cells such as erythrocytes and macrophages can travel, and along which the newly formed axons can regenerate. We suggest that the persistence of these open channels is an important element in the effectiveness of the regeneration. These properties, which the olfactory ensheathing cells exert in collaboration with olfactory nerve fibroblasts, may also be involved in the reparative effects of these cells when transplanted into lesions of the spinal cord.

Animals↗
PubMed1998

LHRH neurons migrate into the trigeminal nerve when the developing olfactory nerve fibers are physically interrupted in chick embryos.

Most LHRH neurons actively migrate from the olfactory epithelium to the forebrain during embryonic days (ED) 3.5-8. When a small piece of the membrane filter was placed on the central course of the olfactory nerve in ED 3.5-5 chick embryos, LHRH neurons deviated from their regular migratory course at ED 6.5-7.5 to follow a route along the PSA-NCAM-positive medial and lateral nasal branches of the ophthalmic nerve of the trigeminal nerve. The olfactory nerve fibers which were specifically immunoreactive for somatostatin also deviated into the ophthalmic nerve. Enzymatic removal of PSA using endoneuraminidase did not interfere with the migration of LHRH neurons into the ophthalmic nerve bundle of the trigeminal nerve. The presence of structural supports seems to be primarily of importance in the migration of LHRH neurons along the olfactory and trigeminal nerve bundles. PSA may be less important for the migration of the LHRH neurons along peripheral neural elements.

Animals↗
PubMed2001

Dopamine D2 receptor-mediated presynaptic inhibition of olfactory nerve terminals.

Olfactory receptor neurons of the nasal epithelium project via the olfactory nerve (ON) to the glomeruli of the main olfactory bulb, where they form glutamatergic synapses with the apical dendrites of mitral and tufted cells, the output cells of the olfactory bulb, and with juxtaglomerular interneurons. The glomerular layer contains one of the largest population of dopamine (DA) neurons in the brain, and DA in the olfactory bulb is found exclusively in juxtaglomerular neurons. D2 receptors, the predominant DA receptor subtype in the olfactory bulb, are found in the ON and glomerular layers, and are present on ON terminals. In the present study, field potential and single-unit recordings, as well as whole cell patch-clamp techniques, were used to investigate the role of DA and D2 receptors in glomerular synaptic processing in rat and mouse olfactory bulb slices. DA and D2 receptor agonists reduced ON-evoked synaptic responses in mitral/tufted and juxtaglomerular cells. Spontaneous and ON-evoked spiking of mitral cells was also reduced by DA and D2 agonists, and enhanced by D2 antagonists. DA did not produce measurable postsynaptic changes in juxtaglomerular cells, nor did it alter their responses to mitral/tufted cell inputs. DA also reduced 1) paired-pulse depression of ON-evoked synaptic responses in mitral/tufted and juxtaglomerular cells and 2) the amplitude and frequency of spontaneous, but not miniature, excitatory postsynaptic currents in juxtaglomerular cells. Taken together, these findings are consistent with the hypothesis that activation of D2 receptors presynaptically inhibits ON terminals. DA and D2 agonists had no effect in D2 receptor knockout mice, suggesting that D2 receptors are the only type of DA receptors that affect signal transmission from the ON to the rodent olfactory bulb.

Animals↗
PubMed1994

Neuropeptide tyrosine is expressed in ensheathing cells around the olfactory nerves in the rat olfactory bulb.

The olfactory bulbs of young and adult normal rats and of colchicine-treated rats and of some other species were analysed for the presence of neuropeptide Y and neuropeptide Y messenger RNA, using immunohistochemistry at the light- and electron-microscopic levels and with in situ hybridization. In the rat and mouse, but not in monkey and guinea-pig, neuropeptide Y-like immunoreactivity and neuropeptide Y messenger RNA were observed in ensheathing cells in the olfactory nerve layer of the olfactory bulb and within nerve bundles in the olfactory mucosa. Double staining experiments revealed that neuropeptide Y-like immunoreactivity was often present in a restricted compartment, mainly the Golgi apparatus, of S-100 protein-positive ensheathing cells. After colchicine treatment a different distribution of neuropeptide Y-like immunoreactivity and neuropeptide Y messenger RNA was observed. Thus, in the outer olfactory nerve layer both neuropeptide Y-like immunoreactivity and neuropeptide Y messenger RNA disappeared, whereas in the inner part messenger RNA levels remained high and neuropeptide Y-like immunoreactivity was observed in many granule-like structures distributed diffusely in the cytoplasm. The present findings suggest that neuropeptide Y may be involved in the control of regeneration, growth and/or guiding of the axons of the olfactory sensory neurons, the only mammalian neurons known to have a continuous renewal and growth during adult life.

Animals↗
PubMed2006

Cytoskeletal organization of the developing mouse olfactory nerve layer.

Olfactory sensory neuron (OSN) axonal extension and targeting occur within the olfactory nerve layer (ONL) of the olfactory bulb (OB). The ONL can be differentiated into sublaminae: the outer (ONLo), where axons broadly target regions of the OB in tight fascicles, and inner (ONLi), where axons perform final targeting in loosely organized fascicles. During perinatal development, cadherin-2 and its binding partner, gamma-catenin, are preferentially expressed by OSN axons in the ONLo vs. the ONLi. Given the expression of these cytoskeleton-associated molecules, we hypothesized that cytoskeletal elements of OSN axons may be differentially expressed across the ONL. We therefore examined cytoskeletal organization of OSN axons in the ONL, focusing on the day of birth (P0). We show that microfilaments, microtubules, and the intermediate filament (IF) vimentin are homogeneously expressed across the ONL at P0. In contrast, the IFs peripherin and alpha-internexin are preferentially localized to the ONLo at P0, with alpha-internexin expressed by a restricted subset of OSNs. We also show that OSN axons in the ONLo are significantly smaller than those in the ONLi. The data demonstrate that, as OSN axons begin to exit the ONLo and target a specific region of the OB, there is a down-regulation of cytoskeletal elements and bound extracellular adhesion molecules. The increase in axon diameter may reflect additional mechanisms involved in glomerular targeting or the formation of the large terminal boutons of OSN axons within glomeruli.

Animals↗
PubMed1997

Glomerular synaptic responses to olfactory nerve input in rat olfactory bulb slices.

In olfactory bulb slices from young rats, the field potential evoked in the glomerular layer by stimulation in the olfactory nerve layer consisted of two negative components: an early component (N1) which was blocked by bath application of the kainate/amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor antagonist 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX, 10 microM), and a late, prolonged component (N2; duration > or = 350 msec) which was unaffected by CNQX, was enhanced by reduction of Mg2+ in the medium, and was blocked by the N-methyl-D-aspartate receptor antagonist DL-2-amino-5-phosphonovalerate (50 microM). A comparison of the glomerular field potentials before and after knife cuts that isolated the glomerular layer from the deeper layers of the olfactory bulb indicated that both N1 and N2 were produced by currents generated, for the most part, within the glomeruli. A laminar analysis of the field potential profiles evoked by olfactory nerve stimulation in standard medium, or in the presence of CNQX, showed that N1 and N2 reversed polarity in the external plexiform and mitral cell layers, suggesting that both components reflected synaptic responses in the distal, apical dendrites of mitral/tufted cells. Simultaneous field potential recordings in the glomerular layer and intracellular recordings in the mitral cell layer showed that: (i) N1 is associated with a brief, short-latency spiking activity of mitral cells, and (ii) N2 is associated with prolonged mitral cell spiking, since N2 and the late cell firing had similar time-courses, and both were blocked by bath applied DL-2-amino-5-phosphonovalerate. Application of the GABA(A) receptor antagonist bicuculline methiodide (10 microM) to standard medium selectively enhanced N2. The enhanced N2 was significantly reduced by DL-2-amino-5-phosphonovalerate. Strychnine, an antagonist of glycine receptors, had similar effects to those of bicuculline, but only at high concentrations that have been previously shown to block GABA(A) receptors; at low concentrations strychnine had no effect. The effects of all drugs tested were reversible. In the rat olfactory bulb, activation of the olfactory nerve evokes a kainate/AMPA receptor-mediated response in the distal, apical dendrites of mitral/tufted cells, followed by a slow N-methyl-D-aspartate receptor-mediated response which triggers prolonged discharge of mitral cells. GABA(A) receptor-mediated inhibition appears to suppress, preferentially, this N-methyl-D-aspartate receptor-mediated component. The presence of prolonged N-methyl-D-aspartate receptor-mediated postsynaptic activity at the primary synapses of the olfactory system may play a key role in olfactory processing by facilitating synaptic integration and plasticity.

Animals↗
PubMed2004

Sensory neuron signaling to the brain: properties of transmitter release from olfactory nerve terminals.

Olfactory receptor neurons (ORNs) convey sensory information directly to the CNS via conventional glutamatergic synaptic contacts in olfactory bulb glomeruli. To better understand the process by which information contained in the odorant-evoked firing of ORNs is transmitted to the brain, we examined the properties of glutamate release from olfactory nerve (ON) terminals in slices of the rat olfactory bulb. We show that marked paired pulse depression is the same in simultaneously recorded periglomerular and tufted neurons, and that this form of short-term plasticity is attributable to a reduction of glutamate release from ON terminals. We used the progressive blockade of NMDA receptor (NMDAR) EPSCs by MK-801 [(5R,10S)-(+)-5-methyl-10,11-dihydro-5H-dibenzo[a,d]cyclohepten-5-10-imine hydrogen maleate] and stationary fluctuation analysis of AMPA receptor (AMPAR) EPSCs to determine the probability of release (P(r)) of ON terminals; both approaches indicated that P(r) is unusually high (>/=0.8). The low-affinity glutamate receptor antagonists gamma-d-glutamylglycine and l-amino-5-phosphonovaleric acid blocked ON-evoked AMPAR- and NMDAR-mediated EPSCs, respectively, to the same extent under conditions of low and high P(r), suggesting that multivesicular release is not a feature of ON terminals. Although release from most synapses exhibits a highly nonlinear dependence on extracellular Ca(2+), we find that the relationship between glutamate release and extracellular Ca(2+) at ON terminals is nearly linear. Our results suggest that ON terminals have specialized features that may contribute to the reliable transmission of sensory information from nose to brain.

Animals↗
PubMed1994

Recovery of olfactory behavior. I. Recovery after a complete olfactory bulb lesion correlates with patterns of olfactory nerve penetration.

The olfactory system is an excellent system in which to study issues related to potential functional recovery after a debilitating brain injury. The olfactory system is well-characterized, easily accessible and there are a vast number of studies available from a variety of perspectives. The experimental aim of this research is to examine the anatomical correlates associated with potential behavioral recovery in rats that receive complete olfactory bulb lesions as neonates or as adults. The results show that behavioral recovery occurs only when olfactory nerve penetration of the central nervous system is observed. Further, both olfactory nerve penetration and behavioral recovery are age-dependent phenomena. The olfactory nerve penetration only occurs when the olfactory bulb lesion is performed in neonates. Behavioral recovery of olfactory ability follows a linear trend and reaches near normal levels during the six weeks behavioral testing period. Histological analysis using an antibody for olfactory marker protein (an olfactory nerve-specific marker) reveals two potential candidates for the anatomical pathway responsible for behavioral recovery: olfactory nerve to orbital frontal cortex and olfactory nerve to olfactory peduncle. This report presents evidence that recovery of olfactory ability can occur in the absence of the olfactory bulb if the lesion is performed when the rat is still a neonate.

Animals↗
PubMed1998

TrkA expression in mouse olfactory tract following axotomy of olfactory nerves.

The olfactory bulb is one of the brain regions that synthesizes the nerve growth factor (NGF). Functional roles of the bulbar NGF remain to be determined. The aim of the present study was, using an antibody specific to the high-affinity NGF receptor (trkA), to examine immunohistochemically the distribution of the NGF receptor in the mouse olfactory tract, under normal conditions and during regenerative processes. In normal mouse olfactory epithelia, trkA immunoreactive cell bodies were only seen in basal cells. Cell bodies of olfactory receptor cells did not express trkA immunoreactivity, but their neuronal processes (olfactory nerve fibres and bundles in the olfactory mucosa and the olfactory bulb) displayed trkA immunoreactivity. After axotomy of olfactory nerves, regenerating olfactory cells (basal cells and olfactory receptor cells) expressed trkA immunoreactivity in intramucosal and intrabulbar neuronal processes of olfactory receptor cells. These results suggest involvement of the bulbar NGF in the process of synaptogenesis and/or regeneration of the olfactory nervous system.

Animals↗
PubMed1985

Immunohistochemical study of subclasses of olfactory nerve fibers and their projections to the olfactory bulb in the rabbit.

The organization of the olfactory nerve projection to the olfactory bulb was studied immunohistochemically in the rabbit by using monoclonal antibodies (MAbs). Out of 42 MAbs raised against the homogenate of the olfactory bulb, two types of MAbs that strongly stained the olfactory nerve fibers (axons of olfactory receptor cells) were selected and their staining patterns were analysed in detail. MAbs of one type (represented by MAb R2D5) specifically labeled all olfactory receptor cells in the nasal epithelium and all olfactory nerve fibers and their terminal portions in the bulb. The other type of MAbs (represented by MAb R4B12) recognized only a subgroup of olfactory nerve fibers. The R4B12-positive fibers were distributed over the ventrolateral areas but not in the dorsomedial areas of the epithelium. Similarly in the bulb, the R4B12-positive fibers terminated in the glomeruli in the ventrolateral and the caudal regions but not in the dorsomedial region. These results demonstrate for the first time the cellular heterogeneity among olfactory receptor neurons at the molecular level. The segregated distribution of the subtypes of olfactory receptor cell axons both in the epithelium and the bulb indicates a defined topographical organization of the olfactory nerve projection. These results also suggest a functional division between dorsomedial and ventrolateral areas both in the epithelium and the bulb.

Afferent Pathways↗
PubMed1993

Purification of olfactory nerve ensheathing cells from the olfactory bulb.

Cells of the olfactory nerve layer of the olfactory bulb are labeled with the O4 antibody, which also labels Schwann cells, oligodendrocytes, and many oligodendrocyte-type-2 astrocyte (O-2A) progenitors. Purification of cells which were O4+, but did not express galactocerebroside (GC), from spinal cord, hippocampus, corpus callosum, and cerebellum of perinatal rats always yielded cells with the expected characteristics of O-2A progenitors. In contrast, the great majority of O4+GC- cells isolated from the olfactory bulb expressed an antigenic phenotype and pattern of differentiation in vitro which did not correspond with that of any previously described glial populations. As the localization of O4 staining in the olfactory bulb indicates that these cells are olfactory nerve ensheathing cells (ONECs), our results therefore suggest that ONECs represent a novel glial cell-type which can now be analyzed as a purified population.

Animals↗