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PubMed2006

Olfactory nerve-evoked, metabotropic glutamate receptor-mediated synaptic responses in rat olfactory bulb mitral cells.

The group I metabotropic glutamate receptor (mGluR) subtype, mGluR1, is highly expressed on the apical dendrites of olfactory bulb mitral cells and thus may be activated by glutamate released from olfactory nerve (ON) terminals. Previous studies have shown that mGluR1 agonists directly excite mitral cells. In the present study, we investigated the involvement of mGluR1 in ON-evoked responses in mitral cells in rat olfactory bulb slices using patch-clamp electrophysiology. In voltage-clamp recordings, the average EPSC evoked by single ON shocks or brief trains of ON stimulation (six pulses at 50 Hz) in normal physiological conditions were not significantly affected by the nonselective mGluR antagonist LY341495 (50-100 microM) or the mGluR1-specific antagonist LY367385 (100 microM); ON-evoked responses were attenuated, however, in a subset (36%) of cells. In the presence of blockers of ionotropic glutamate and GABA receptors, application of the glutamate uptake inhibitors THA (300 microM) and TBOA (100 microM) revealed large-amplitude, long-duration responses to ON stimulation, whereas responses elicited by antidromic activation of mitral/tufted cells were unaffected. Magnitudes of the ON-evoked responses elicited in the presence of THA-TBOA were dependent on stimulation intensity and frequency, and were maximal during high-frequency (50-Hz) bursts of ON spikes, which occur during odor stimulation. ON-evoked responses elicited in the presence of THA-TBOA were significantly reduced or completely blocked by LY341495 or LY367385 (100 microM). These results demonstrate that glutamate transporters tightly regulate access of synaptically evoked glutamate from ON terminals to postsynaptic mGluR1s on mitral cell apical dendrites. Taken together with other findings, the present results suggest that mGluR1s may not play a major role in phasic responses to ON input, but instead may play an important role in shaping slow oscillatory activity in mitral cells and/or activity-dependent regulation of plasticity at ON-mitral cell synapses.

Amino Acids↗
PubMed1988

Olfactory neural pathway in mouse hepatitis virus nasoencephalitis.

The mechanism of brain infection with mouse hepatitis virus-JHM was studied in BALB/cByJ mice following intranasal inoculation, and found to be a consequence of direct viral spread along olfactory nerves into olfactory bulbs of the brain. Infection was followed sequentially from nose to brain, using microscopy, immunohistochemistry and virus quantification. Lesions, antigen and virus were observed in the olfactory bulb and anterior brain as early as 2 days and posterior brain by 4 days after inoculation. Viral antigen extended through nasal mucosa into submucosa, then coursed along the olfactory nerve perineurium and fibers, through the cribriform plate into the olfactory bulbs. On days 4 and 7, viral antigen was found in the antero-ventral brain, along ventral meninges, olfactory tracts and anterior ramifications of the lateral ventricles. Virus was cleared from nose by 10 days and anterior brain by 20 days, but persisted in posterior brain for 20 days after inoculation. Mice also developed disseminated infection, with viremia and hepatitis. Infection of brain did not correlate with presence of viremia. In contrast to intranasally inoculated mice, orally-inoculated mice did not develop encephalitis, despite evidence of disseminated infection.

Animals↗
PubMed1993

Ensheathing cells in the nerve fiber layer of the olfactory bulb--a novel glial cell type.

Olfactory nerve ensheathing cells (ONECs) were originally described as Schwann cells of the olfactory nerve. More recent studies have suggested that these cells express features of astrocytes, including the lack of basal lamina and collagen fibrils and the failure to ensheath axons individually. Recently performed experimental studies showed that ONECs from the olfactory bulb represent a novel glial cell type.

Animals↗
PubMed2000

Gonadotropin-releasing hormone-immunoreactive neurons and associated nicotinamide adenine dinucleotide phosphate-diaphorase-positive neurons in the brain of a teleost, Rhodeus amarus.

Using combined nicotinamide adenine dinucleotide phosphate-diaphorase (NADPHd) histochemistry and salmon gonadotropin-releasing hormone (sGnRH) immunocytochemistry, it is reported for the first time that possible potential contacts occur between the nitric oxide (NO)- and the GnRH-containing neurons in the brain of a freshwater teleost, Rhodeus amarus. GnRH-immunoreactive (ir) neurons were observed in the olfactory nerve (OLN), olfactory bulb (OB), medial olfactory tract (MOT), ventral telencephalon (VT), nucleus preopticus periventricularis (NPP), nucleus lateralis tuberis (NLT), and midbrain tegmentum (MT). Although NADPHd neurons were widely distributed in the brain, only those having an association with GnRH-ir neurons are described. Based on the nature of the association between the GnRH and the NADPHd neurons, the former were classified into three types. The Type I GnRH neurons were characterized by the presence of NADPHd-positive granules in the perikarya and processes and occurred in the OLN, OB, MOT, and VT. The Type II GnRH neurons, having soma-soma or soma-process contacts with the NADPHd neurons, were restricted to the MT; the long processes of NADPHd cells crossed over either the perikarya or the thick processes of GnRH cells. However, the Type III GnRH neurons, found in the NPP and NLT, did not show direct contact, but a few NADPHd fibers were present in the vicinity. The terminal-soma contacts in the olfactory system and the VT and the soma-soma contacts in the MT represent the sites of possible potential contacts indicating a direct NO involvement in GnRH function, although NO action by diffusion remains possible. NO may influence the NPP and NLT GnRH cells by diffusion only, since a direct contact was not observed.

Animals↗
PubMed1992

Luteinizing hormone-releasing hormone in the pigeon terminal nerve and olfactory bulb.

The presence of a terminal nerve in the avian brain has recently been reported. As the terminal nerve in other classes of vertebrates contains luteinizing hormone-releasing hormone (LHRH), we used immunocytochemistry to determine whether the pigeon terminal nerve also contained LHRH. We found LHRH-immunoreactivity in the olfactory nerve and in the olfactory bulb. The distribution of LHRH neurons was similar to the LHRH neuronal migration pathway during development.

Animals↗
PubMed1994

Ultrastructural demonstration of salmon-type gonadotropin-releasing hormone (sGnRH) in the olfactory system of masu salmon (Oncorhynchus masou).

Immunocytochemical and immunoelectron microscopic localization of salmon-type gonadotropin-releasing hormone (sGnRH) were observed in the olfactory system (olfactory epithelium, olfactory nerve and olfactory bulb) of masu salmon (Oncorhynchus masou) to investigate its possible involvement in the olfactory functions. sGnRH-immunoreactive (ir) bipolar neuron, which might be related to the terminal nerve, was located in dorsal portion of the olfactory nerve. sGnRH-ir gold particles were concentrated on electron-dense granule-like structures of 50 nm in diameter in fibers of the olfactory nerve close both to the olfactory epithelium and to the olfactory bulb. These findings suggest that sGnRH might participate in neurotransmission and/or neuromodulation in the olfactory system of masu salmon. sGnRH would become a useful molecular marker for studying the olfactory imprinting and homing mechanisms in salmonids.

Animals↗
PubMed1981

Primary afferent depolarization in the in vitro frog olfactory bulb.

1. Experiments on the frog olfactory bulb have been performed in vitro in order to determine whether primary afferent transmission is modified by presynaptic inhibition.2. Stimulation of the olfactory nerve resulted in a prolonged depolarization of the olfactory nerve as recorded across a sucrose gap. Unstimulated olfactory nerve fibres adjacent to the stimulated fibres were also depolarized.3. An excitability increase of the olfactory nerve terminals was found that lasted the entire duration of the olfactory nerve depolarization, indicating that the terminals themselves were depolarized. Both the olfactory nerve depolarization and the excitability increase were blocked by cobalt and manganese ions.4. Low concentrations of glutamate were found to produce a substantial depolarization of the olfactory nerve. Although gamma-aminobutyric acid (GABA) also elicited a depolarization of the olfactory nerve, picrotoxin, a GABA antagonist, did not reduce the stimulus-evoked olfactory nerve depolarization.5. Recording with potassium-sensitive electrodes in the olfactory nerve terminal region demonstrated an increase in extracellular potassium with the same rise time and duration as the olfactory nerve depolarization. Cobalt and manganese blocked the potassium increase and the olfactory nerve depolarization without affecting the presynaptic action potential.6. The focally recorded extracellular current resulting from orthodromic synaptic excitation of the secondary olfactory relay neurones was blocked at short intervals by paired stimulation and decreased for the duration of the olfactory nerve depolarization. This suggests a decreased release of transmitter from the olfactory nerve terminals.7. The possible role of potassium and/or a neurotransmitter in generating the olfactory nerve depolarization and inhibition is discussed.

Animals↗
PubMed1992

Immunocytochemical identification of primary olfactory afferents in rainbow trout.

We have used a combination of techniques to analyze the primary olfactory projection in trout: anterograde tract tracing with horseradish peroxidase (HRP) and immunocytochemistry with antisera to olfactory marker protein (OMP) and to keyhole limpet hemocyanin (KLH). HRP labeling and the OMP antiserum revealed a subset of ciliated receptor neurons with a wide dendrite that lacked the protruding knob found on other receptor neurons. The organization of the primary olfactory axons was clearly revealed by antisera to KLH, which reacted with no other neurons. When visualized with anti-KLH, fascicles of olfactory axons penetrated the basal lamina of the olfactory rosette at scattered sites and converged to form the olfactory nerve. Fascicles within the olfactory nerve traveled parallel to the long axis of the nerve until resorted by extensive intermixing as they entered the olfactory bulb. Within the olfactory bulb, most axons terminated in nine discrete terminal fields in the glomerular layer; however, a few olfactory nerve axons projected into the ventral medial telencephalon. Fascicles supplying each terminal field in the glomerular layer followed distinctive trajectories within the olfactory nerve layer. Axons ending in two terminal fields made brush-like terminations rather than the glomerular terminations characteristic of the remaining seven fields. After unilateral olfactory nerve transection, returning olfactory axons reestablished the normal pattern of terminal fields within 14 weeks. It is likely that the organization of afferents in the trout olfactory bulb is similarly well regulated during normal receptor cell replacement.

Animals↗
PubMed2002

Specificity of glomerular targeting by olfactory sensory axons.

Axons from olfactory sensory neurons (OSNs) expressing a specific odorant receptor (OR) project to specific subsets of glomeruli in the olfactory bulb (for review, see Mombaerts, 1999, 2001). The aim of this study was to examine the trajectories that subsets of axons from OSNs expressing the same OR follow within the olfactory nerve and olfactory nerve layer (ONL) of adult mice. Using confocal microscopy, we generated serial reconstructions of axons from M72-IRES-tauGFP-expressing OSNs as they coursed within the ONL and into glomeruli. GFP-expressing axons were loosely aggregated in the outer ONL; however, as they entered the inner ONL, the majority fasciculated with other GFP-expressing axons before entering the glomerular neuropil. Although the vast majority of axons entered the glomerulus from the directly apposed ONL, some followed tortuous courses through and/or around adjacent glomeruli before terminating in the target glomerulus. Similar observations were made on subpopulations of axons in M71-IRES-tauGFP and P2-IRES-tauGFP mice. Ultrastructural analyses of labeled M72 glomeruli showed no evidence of axodendritic synapses other than those with GFP-labeled axon terminals. These data are consistent with the notion that OSN axons are highly precise in targeting glomeruli and that glomeruli, in turn, are highly homogeneous with regard to the OR expressed by the innervating OSNs. Because some single axons could follow idiosyncratic trajectories to the target glomerulus, it appears that stable homotypic fasciculation is not a prerequisite for correct targeting.

Animals↗
PubMed2000

Enzymatic removal of polysialic acid from neural cell adhesion molecule perturbs the migration route of luteinizing hormone-releasing hormone neurons in the developing chick forebrain.

During development in the chick embryo, luteinizing hormone-releasing hormone (LHRH) neurons migrate along the olfactory nerve from the olfactory epithelium to the forebrain. At embryonic day 5.5 (E5.5) to E6.0, the majority of LHRH neurons begin to enter the medial forebrain and then course dorsocaudally along the forebrain substance just beneath the pia matter in association with the somatostatin (SST)-positive fibers, which branch medially from the SST-positive olfactory nerve. By E6.5, the neurons and SST-positive medial branch of the olfactory nerve have proceeded toward the septal area. Intense immunoreactivity for the polysialylated form of neural cell adhesion molecule (PSA-NCAM) on both the LHRH neurons and the SST-positive fibers during this period suggests that this less adhesive form of NCAM is involved in the migratory process. This possibility was examined by using a polysialic acid (PSA)-specific endoneuraminidase. PSA removal did not alter the behavior or appearance of the SST-positive olfactory fibers within the migration pathway. However, it induced a significant deviation of migrating LHRH neurons from the regular path in the forebrain. The effect of PSA removal is more likely to involve changes in the interaction of the migrating neurons with a subset of the SST-positive olfactory fibers and/or other elements in the forebrain rather than an alteration in the pattern of their axonal substrate. On the basis of these results, it is suggested that PSA contributes to the specific pattern of LHRH neuronal migration in the forebrain by limiting interaction of these LHRH neurons with their surrounding environment.

Animals↗
PubMed2005

[Clinical anatomy study of olfaction correlative nerves].

OBJECTIVE: To find out the relation of the olfactory nerves, the optic nerve, and the nasal sinuses. Provide anatomic data for not to damnify olfactory nerves in the surgery. METHOD: To measure the olfactory nerves, the olfactory bulb, and olfactory tract on 16 adult cadaveric specimens, and observe the relation of the olfactory nerves, the optic nerve,and the nasal sinuses. RESULT: Length of the olfactory tract was (29.32 +/- 2.11) mm, width of the olfactory tract was (3.36 +/- 0.83) mm. The distance from the midpoint of the olfactory tract to the midline of the skull was (5.48 +/- 1.02) mm. The angle between olfactory tract and midline of the skull was (21.32 +/- 3.28) degrees. Length of the olfactory bulb was (10.43 +/- 2.35) mm, width of the olfactory bulb was (5.12 +/- 0.62) mm. 27/32 olfactory tracts were border upon with sphenoid sinus and ethmoid sinus, 3/32 olfactory tracts were border upon with ethmoid sinus, 2/32 olfactory tracts were border upon with frontal sinus. All olfactory tracts crossed the optic nerve at the internal meatus of optic nerve canal. The olfactory bulb and ethmoid bulb were on equal line. CONCLUSION: Almost all olfactory tracts were lied in the inboard of the orbital cavity, protect the roof of the nasal sinus to avoid damnify the olfactory nerves. It is easy to pull out the olfactory nerves when raising the cerebra in the operation of anterior cranial fossae.

Adult↗
PubMed1993

Effects of chronic low-level copper exposure on ultrastructure of the olfactory system in rainbow trout (Oncorhynchus mykiss).

This study investigated the effects of a chronic exposure to a low level of copper on cell populations of the olfactory system in yearling rainbow trout. Fish were sacrificed after 15, 30 and 60 days of copper exposure. Transmission electron microscopy was used to describe the sequence of subcellular changes occurring in three tissues, the sensory epithelium, the olfactory nerve and the olfactory bulb. Data show that a 15-day exposure to 20 micrograms/l of copper causes specific degeneration of all mature receptor cells as well as numerous immature neurons. Moreover, degenerating receptor cells exhibited morphological features of a cell death by apoptosis. After 30 days, and more specifically after 60 days of exposure, numerous clusters of cells were observed in the basal region of the epithelium, suggesting a great mitotic activity in this area. In parallel, an increased number of maturing receptor cells and goblet cells were observed, but no fully mature neurons were noted even after 60 days of exposure. In both the olfactory nerve and the olfactory bulb, the number of degenerating axons and terminals, which was high at 15 days, decreased with time and some process of glomerular reinnervation was detected after 60 days. A reactive hypertrophy of supporting, ensheathing and astrocytic cells was also observed in exposed fish, which demonstrates that these cell types are actively involved in the process of tissue scarring. Even though some signs of neuronal regeneration were reported during the time-course of exposure, indicating some fish acclimation, results raise the question of the olfactory function during such environmental stress.

Animals↗
PubMed1987

Locus coeruleus stimulation modulates olfactory bulb evoked potentials.

Field-evoked potentials from the main olfactory bulb in response to stimulation of the olfactory nerve and lateral olfactory tract were measured without and with conditioning stimulation of the locus coeruleus noradrenergic system. The locus coeruleus conditioning stimulus suppressed or inhibited the late components of the olfactory bulb potential evoked by orthodromic olfactory nerve stimulation; this inhibitory effect was suppressed by the microinjection of the alpha-adrenergic blocker prazosin into the olfactory bulb. Results indicate that noradrenergic fibers projecting from the locus coeruleus exert modulatory influences on neuronal networks underlying orthodromic evoked responses in the main olfactory bulb.

Adrenergic Fibers↗
PubMed2004

Translocation of inhaled ultrafine particles to the brain.

Ultrafine particles (UFP, particles <100 nm) are ubiquitous in ambient urban and indoor air from multiple sources and may contribute to adverse respiratory and cardiovascular effects of particulate matter (PM). Depending on their particle size, inhaled UFP are efficiently deposited in nasal, tracheobronchial, and alveolar regions due to diffusion. Our previous rat studies have shown that UFP can translocate to interstitial sites in the respiratory tract as well as to extrapulmonary organs such as liver within 4 to 24 h postexposure. There were also indications that the olfactory bulb of the brain was targeted. Our objective in this follow-up study, therefore, was to determine whether translocation of inhaled ultrafine solid particles to regions of the brain takes place, hypothesizing that UFP depositing on the olfactory mucosa of the nasal region will translocate along the olfactory nerve into the olfactory bulb. This should result in significant increases in that region on the days following the exposure as opposed to other areas of the central nervous system (CNS). We generated ultrafine elemental (13)C particles (CMD = 36 nm; GSD = 1.66) from [(13)C] graphite rods by electric spark discharge in an argon atmosphere at a concentration of 160 microg/m(3). Rats were exposed for 6 h, and lungs, cerebrum, cerebellum and olfactory bulbs were removed 1, 3, 5, and 7 days after exposure. (13)C concentrations were determined by isotope ratio mass spectroscopy and compared to background (13)C levels of sham-exposed controls (day 0). The background corrected pulmonary (13)C added as ultrafine (13)C particles on day 1 postexposure was 1.34 microg/lung. Lung (13)C concentration decreased from 1.39 microg/g (day 1) to 0.59 microg/g by 7 days postexposure. There was a significant and persistent increase in added (13)C in the olfactory bulb of 0.35 microg/g on day 1, which increased to 0.43 microg/g by day 7. Day 1 (13)C concentrations of cerebrum and cerebellum were also significantly increased but the increase was inconsistent, significant only on one additional day of the postexposure period, possibly reflecting translocation across the blood-brain barrier in certain brain regions. The increases in olfactory bulbs are consistent with earlier studies in nonhuman primates and rodents that demonstrated that intranasally instilled solid UFP translocate along axons of the olfactory nerve into the CNS. We conclude from our study that the CNS can be targeted by airborne solid ultrafine particles and that the most likely mechanism is from deposits on the olfactory mucosa of the nasopharyngeal region of the respiratory tract and subsequent translocation via the olfactory nerve. Depending on particle size, >50% of inhaled UFP can be depositing in the nasopharyngeal region during nasal breathing. Preliminary estimates from the present results show that approximately 20% of the UFP deposited on the olfactory mucosa of the rat can be translocated to the olfactory bulb. Such neuronal translocation constitutes an additional not generally recognized clearance pathway for inhaled solid UFP, whose significance for humans, however, still needs to be established. It could provide a portal of entry into the CNS for solid UFP, circumventing the tight blood-brain barrier. Whether this translocation of inhaled UFP can cause CNS effects needs to be determined in future studies.

Air Pollutants↗
PubMed2002

Neural regeneration and the peripheral olfactory system.

The peripheral olfactory system is able to recover after injury, i.e., the olfactory epithelium reconstitutes, the olfactory nerve regenerates, and the olfactory bulb is reinnervated, with a facility that is unique within the mammalian nervous system. Cell renewal in the epithelium is directed to replace neurons when they die in normal animals and does so at an accelerated pace after damage to the olfactory nerve. Neurogenesis persists because neuron-competent progenitor cells, including transit amplifying and immediate neuronal precursors, are maintained within the population of globose basal cells. Notwithstanding events in the neuron-depleted epithelium, the death of both non-neuronal cells and neurons directs multipotent globose basal cell progenitors, to give rise individually to sustentacular cells and horizontal basal cells as well as neurons. Multiple growth factors, including TGF-alpha, FGF2, BMPs, and TGF-betas, are likely to be central in regulating choice points in epitheliopoiesis. Reinnervation of the bulb is rapid and robust. When the nerve is left undisturbed, i.e., by lesioning the epithelium directly, the projection of the reconstituted epithelium onto the bulb is restored to near-normal with respect to rhinotopy and in the targeting of odorant receptor-defined neuronal classes to small clusters of glomeruli in the bulb. However, at its ultimate level, i.e., the convergence of axons expressing the same odorant receptor onto one or a few glomeruli, specificity is not restored unless a substantial number of fibers of the same type are spared. Rather, odorant receptor-defined subclasses of neurons innervate an excessive number of glomeruli in the rough vicinity of their original glomerular targets.

Animals↗
PubMed1994

The arrest of luteinizing hormone-releasing hormone neuronal migration in the genetic arhinencephalic mouse embryo (Pdn/Pdn).

From previous observations, it was suggested that non-attachment of the olfactory nerve to the telencephalon blocked the induction of the olfactory bulbs in genetic arhinencephalic mouse embryos (Pdn/Pdn). The olfactory nerve ends in a tangle beneath the forebrain in these embryos. From these observations, we speculated that the migration of luteinizing hormone-releasing hormone (LHRH) neurons might be disturbed in the olfactory nerve. A mass of LHRH neurons was observed in the end of the olfactory nerve fibers, but LHRH neurons were found in the hypothalamus in Pdn/Pdn embryos on day 16 of gestation. Narrow by-paths were found between the olfactory nerve and the forebrain, and the migration of LHRH neurons through these by-paths was observed in Pdn/Pdn embryos on day 13 of gestation. From the reports that a gene deleted in the arhinencephalic syndrome (Kallmann's syndrome) shares homology with neural cell adhesion molecules (N-CAM), it was speculated that non-attachment of the olfactory nerve in the Pdn/Pdn embryo might be associated with abnormalities of N-CAM. The axon fibers of the olfactory nerve reacted specifically with anti-N-CAM IgG both in +/- (+/+ and/or Pdn/+) and Pdn/Pdn on day 11.5 and 12, but not on day 13 and 16 of gestation. The axon fibers of the olfactory nerve were positive to anti-N-CAM IgG specifically just during the developmental period that the olfactory nerve fibers attached to the telencephalon. It is still not clear whether non-attachment of the olfactory nerve may be associated with N-CAM or not from the present observations.

Animals↗
PubMedDate not supplied

Isoproterenol increases CREB phosphorylation and olfactory nerve-evoked potentials in normal and 5-HT-depleted olfactory bulbs in rat pups only at doses that produce odor preference learning.

Norepinephrine (NE) and serotonin (5-HT) are important modulators of early odor preference learning. NE can act as an unconditioned stimulus (UCS), whereas 5-HT facilitates noradrenergic actions. In this study, we examined the phosphorylation of an important transcription factor, cAMP response element binding protein (CREB), which has been implicated in long-term-memory formation (McLean et al. 1999) during NE-induced odor preference learning in normal and olfactory bulb 5-HT-depleted rat pups. We also examined NE modulation of olfactory nerve-evoked field potentials (ON-EFPs) in anesthetized normal and bulbar 5-HT depleted pups. Systemic injection of 2 mg/kg isoproterenol (beta-adrenoceptor agonist) induced odor preference learning, enhanced pCREB expression in the olfactory bulbs at 10 min after odor pairing, and increased ON-EFPs in normal rat pups but not in bulbar 5-HT-depleted rat pups. A dose of 6 mg/kg isoproterenol, which was ineffective in modulating these measures in normal rat pups, induced odor preference learning, enhanced phosphorylated CREB (pCREB) expression, and increased ON-EFPs in bulbar 5-HT-depleted pups. These outcomes suggest that NE and 5-HT promote specific biochemical and electrophysiological changes that may critically underlie odor preference learning.

Animals↗