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PubMed1993

Evidence for presynaptic inhibition of the olfactory commissural pathway by cholinergic agonists and stimulation of the nucleus of the diagonal band.

We have investigated the role of the projection from the magnocellular basal forebrain to the olfactory bulb in regulating synaptic transmission in the commissural connection between the two olfactory bulbs. Commissural fibers arise in the contralateral anterior olfactory nucleus, travel in the anterior wing of the anterior commissure (AC), and terminate in the granule cell layer of the olfactory bulb. Electrical stimulation of the commissure causes synaptic activation of granule cells in the granule cell layer of the bulb; the resulting field potential is a reliable indicator of this synaptic current. Microinjections of cholinergic agonists, but not of identical, or larger, quantities of vehicle, reduced the amplitude of this AC field potential. Systemic injection of scopolamine reversed this depression and returned the AC response amplitude to control levels. Irreversible AChE inhibition also reduced the amplitude of the AC response, and muscarinic blockade reversed this effect. Cholinergic terminals in the olfactory bulb arise entirely from the axons of magnocellular basal forebrain neurons in the nucleus of the diagonal band (NDB). Electrical stimulation of NDB, which should release ACh, as well as other transmitters, depressed the AC response. Brief trains of NDB shocks caused a moderate decrease in the AC response that lasted 1-2 sec. Longer shock trains, which caused marked potentiation of the NDB field potential, caused a profound, prolonged (> 20 sec) inhibition of the AC response. Antidromic tests demonstrated that NDB stimulation significantly decreased the excitability of AC terminals. This and other characteristics of the inhibition strongly suggest that the decrease in amplitude of the field potential response to AC stimulation caused by cholinergic agonists and stimulation of NDB is due to presynaptic inhibition leading to reduced release of transmitter from AC terminals. These results suggest that one function of the basal forebrain projection to the olfactory bulb is inhibition of the commissural connection between the two olfactory bulbs. As NDB has been implicated in theta pacemaker input to the olfactory bulb, phasic NDB inhibition of centrifugal afferents to the bulb could function to coordinate signal processing temporally in the olfactory system. Temporal coordination may be particularly important to olfactory circuit function, as this system lacks the point-to-point topographical organization characteristic of other sensory systems.

Acetylcholine↗
PubMed2002

Neurotrophins and their receptors in the primary olfactory neuraxis.

The primary olfactory pathway is an elegant and simple system in which to study neurogenesis and neuronal plasticity because of the simple fact that olfactory receptor neurons (ORNs) are continually generated throughout the adult lifetimes of vertebrates. Thus, neuronal birth, differentiation, survival, axon pathfinding, target recognition, synapse formation, and cell death are developmental events that can be examined in the mature olfactory epithelium (OE). Neurotrophins (nerve growth factor, brain-derived neurotrophic factor, and neurotrophin 3, and 4/5) are a family of bioactive peptides that exert their effects by interacting with high- and low-affinity receptors on the surfaces of responsive cells, and have been implicated in several stages of neuronal development throughout the central and peripheral nervous system (CNS and PNS). There has been significant interest within the olfactory community as to how these multifunctional peptides might regulate the cycle of degeneration and regeneration of olfactory receptor neurons. The focus of this review is to highlight what is known about the actions of neurotrophins in the primary olfactory pathway, and to pinpoint future directions that will enable us to further understand their role in olfactory receptor neuron development and turnover.

Animals↗
PubMed2002

A study of systems for delivering antigens and plasmid DNA for intranasal immunization against tick-borne encephalitis virus.

Our previous studies indicated the possibility for some neurotropic viruses to spread into the brain of immune animals through the olfactory pathway. Thus, nasal mucosa in the olfactory region is likely to be a promising target for mucosal immunization to protect the CNS from neurotropic viral infections. THE MAIN IDEA OF THE RESEARCH: Intranasal immunization inducing mucosal and systemic immune responses blocks the propagation of neurotropic virus into the brain via the olfactory pathway and neutralizes the multiplication of virus in visceral organs, allowing more effective protection against neurotropic infections transmitted by bloodsucking arthropods to be achieved. Thus, study of the efficiency of delivery systems for intranasal immunization against tick-borne encephalitis (TBE) virus is an urgent task in the development of anti-TBE mucosal vaccine. To study intranasal immunization against TBE virus, we have chosen four delivery systems (DSs), namely, (i) biodegradable microparticles, (ii) cationic liposomes, and live attenuated (iii) bacterial and (iv) viral vectors. The gene of TBE virus protein E was inserted into the pcDNA3 plasmid (designated as pcDNA3/E-TBE). Three types of delivery system for plasmid DNA were developed and studied in vitro. The first system, artificial virus-like microparticles (VLP), consists of polyglycan-spermidine complexes that cover pcDNA3/E-TBE DNA. The second system is cationic liposomes with DNA of the plasmid pcDNA3/E-TBE. The third system is an attenuated Salmonella strain containing pcDNA3/E-TBE. The fourth system is a recombinant vaccinia strain with inserted genes of TBE virus proteins C, prM, E, NS1, NS2a, NS2b, and NS3. The DSs were tested in COS-7 and CV-1 cell lines and macrophages by ELISA of cell lysate. The results obtained showed the expression of the E gene in transfected cells, thereby demonstrating that these DSs are suitable for mucosal immunization. High levels of immune response shifted to the Th1 type were detected in BALB/c mice following intranasal immunization with recombinant vaccinia-TBE strain and VLP-pcDNA3/E-TBE. The mice immunized intranasally with recombinant vaccinia-TBE strains were completely protected against intraperitoneal challenge with TBE virus strain Sofjin, whereas intranasal immunization with killed TBE vaccine failed to induce a significant level of protection.

Administration, Intranasal↗
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↗
PubMed2004

Glycosylation patterns are sexually dimorphic throughout development of the olfactory system in Manduca sexta.

In the moth Manduca sexta, development of the adult olfactory system depends on complex interactions between olfactory receptor neurons in the antenna, antennal-lobe neurons in the brain, and several classes of glial cells. As one approach to characterizing molecules that may play roles in these interactions, we used lectins to screen antennae and antennal lobes at different stages of adult development. We find that each of the major neural cell types has a distinct pattern of labeling by lectins. Effects of enzymatic and other treatments on lectin labeling lead us to conclude that the predominant lectin ligands are: glycosphingolipids and an O-linked, fucose-containing glycoprotein on axons of olfactory receptor neurons, O-linked glycoproteins on antennal-lobe neurons, and N-linked glycoproteins on all classes of glial cells in the primary olfactory pathway. Wheat germ agglutinin labels all olfactory axons uniformly during much of development, but labeling becomes restricted to the pheromone-responsive olfactory receptor neurons in the adult male. Succinylated WGA reveals differences in these axon classes earlier, as glomerului develop from protoglomeruli. The adult female displays a less pronounced difference in labeling of axons targeting ordinary and sexually dimorphic glomeruli. Differences in labeling of receptor axons targeted to ordinary and sexually dimorphic glomeruli may be correlated with differences in function or connectivity in different regions of the antennal lobe.

Animals↗
PubMedDate not supplied

Axonal loss from the olfactory tracts in Alzheimer's disease.

Senile dementia of the Alzheimer type has been shown to be associated with impaired olfactory function early in the course of the disease. Neuropathology in the olfactory system is also a feature of Alzheimer's disease (AD) and it has been suggested that the disease may be caused by a pathogen entering the brain via olfactory pathways. To investigate this hypothesis, the effect of AD on the olfactory tract was investigated. There was a 40% decrease in the cross-sectional area of the olfactory tract and a 52% loss of myelinated axons from the tract in AD. These results, together with those of previous studies suggest that peripheral regions of the olfactory system, i.e., the olfactory bulb and primary sensory olfactory neurons are less affected by the pathology of AD than more central parts, i.e., cortical regions, the anterior olfactory nuclei, and olfactory tract. This less severe pathology at the periphery argues against a pathogen entering the brain via the peripheral olfactory apparatus and suggests a central pathogenesis which spreads centrifugally along olfactory pathways.

Aged↗
PubMedDate not supplied

Elements of the olfactory signaling pathways in insect antennae.

Owing to their enormous ability to recognize airborne molecules, insects have long been used as model systems for studying various aspects of olfaction. Modern biological techniques have opened new avenues for exploring the molecular mechanisms underlying the complex signaling processes in chemosensory neurons. Biochemical and molecular analyses have allowed the identification of molecular elements of the olfactory reaction pathways and have shed light on mechanisms that account for the sensitivity and specificity of the chemosensory system.

Amino Acid Sequence↗
PubMed2006

Variations in the human olfactory receptor pathway.

Of all five senses, olfaction is the most complex molecular mechanism, as it comprises hundreds of receptor proteins enabling it to detect and discriminate thousands of odorants. Until lately, the understanding of this highly sophisticated sensory neuronal pathway has been rather sketchy. The sequencing of the human genome and the consequent advent of new genomic tools have opened new opportunities to better understand this multifaceted biological system. Here, we present the relevant progresses made in the last decade and highlight the possible genetic mechanisms of human olfactory variability.

Animals↗
PubMed2004

Balamuthia mandrillaris, an opportunistic agent of granulomatous amebic encephalitis, infects the brain via the olfactory nerve pathway.

Balamuthia mandrillaris is a free-living ameba and an opportunistic agent of lethal granulomatous amebic encephalitis (GAE) in humans and other mammals. Its supposed routes of infection have been largely assumed from what is known about Acanthamoeba spp. and Naegleria fowleri, other free-living amebae and opportunistic encephalitis agents. However, formal proof for any migratory pathway, from GAE patients or from animal models, has been lacking. Here, immunodeficient mice were infected with B. mandrillaris amebae by intranasal instillation, the most likely natural portal of entry. By means of classical and immunohistology, the amebae are shown to adhere to the nasal epithelium, progress along the olfactory nerves, traverse the cribriform plate of the ethmoid bone, and finally infect the brain. A similar invasion pathway has been described for N. fowleri. The data suggest that the olfactory nerve pathway is a likely route for natural infection of the brain by B. mandrillaris amebae.

Amebiasis↗
PubMed2003

Axon mis-targeting in the olfactory bulb during regeneration of olfactory neuroepithelium.

During development, primary olfactory axons typically grow to their topographically correct target zone without extensive remodelling. Similarly, in adults, new axons arising from the normal turnover of sensory neurons essentially project to their target without error. In the present study we have examined axon targeting in the olfactory pathway following extensive chemical ablation of the olfactory neuroepithelium in the P2-tau:LacZ line of mice. These mice express LacZ in the P2 subpopulation of primary olfactory neurons whose axons target topographically fixed glomeruli on the medial and lateral surfaces of the olfactory bulb. Intraperitoneal injections of dichlobenil selectively destroyed the sensory neuroepithelium of the nasal cavity without direct physical insult to the olfactory neuron pathway. Primary olfactory neurons regenerated and LacZ staining revealed the trajectory of the P2 axons. Rather than project solely to their topographically appropriate glomeruli, the regenerating P2 axons now terminated in numerous inappropriate glomeruli which were widely dispersed over the olfactory bulb. While these errors in targeting were refined over time, there was still considerable mis-targeting after four months of regeneration.

Aging↗
PubMed1982

Contacts of pore tubules and sensory dendrites in antennal chemosensilla of a silkmoth: demonstration of a possible pathway for olfactory molecules.

Antennal olfactory hairs of Antheraea polyphemus were investigated by means of transmission electron microscopy. Adequate preservation of dendrites and extracellular pore tubules is obtained by mechanical opening of the hair lumen and subsequent chemical fixation. The dendritic membrane has a cell coat. The dendrites contain microfilamentous structures in addition to their cytoplasmatic microtubules. The extracellular pore tubules traverse the hair cuticle and reach into the hair lumen for maximally 350 nm. Their diameter varies between 20 and 40 nm, depending on the preparation method. They consist of an electron-dense wall and an electron-lucent core. The wall has a helical substructure and is covered with a fuzzy coat. Contacts of pore tubules and dendritic membranes occur wherever dendrites are near the inner surface of the hair cuticle. Some of the pore tubules terminate approximately at right angles on the dendritic membrane, others lie against the membrane. The contact seems to be made via the surface coats of the tubules and the membrane. The structure of pore tubules which had been negatively stained with uranyl acetate is similar to the conventionally thin-sectioned material. The observations provide support for earlier assumptions that pore tubules are the pathways by which odor molecules reach the dendritic membrane.

Animals↗
PubMed2003

The contribution of signaling pathways to olfactory organization and development.

The exquisite specificity in the organization of the mammalian olfactory system underlies its remarkable sensitivity and precision in odorant detection. The contribution of olfactory receptor proteins to the initial patterning of connections between the sensory epithelium and the bulb is widely appreciated. The application of genetic model systems has revealed additional roles for odorant-evoked activity in the development, organization and dynamic turnover of cells in this regenerating sensory organ.

Animals↗
PubMed1997

Sex hormones enhance the impact of male sensory cues on both primary and association cortical components of visual and olfactory processing pathways as well as in limbic and hypothalamic regions in female sheep.

Differential activation of neural substrates was investigated in female sheep exposed to a male when they were in oestrus, and sexually receptive and attracted to males, as opposed to anoestrus when they were not. Changes in neuronal activation were visualized in ovariectomized, hormone-treated ewes by quantifying changes in cellular expression of c-fos messenger RNA by in situ hybridization histochemistry. Results showed that, while oestrus induction had no significant effects on c-fos expression per se, a 5-min exposure to a male significantly increased it in a number of primary and association cortical regions (the mitral and granule cell layers of the olfactory bulb, visual, somatosensory, orbitofrontal, piriform, cingulate and temporal cortices), the limbic system (CA1 region of the hippocampus, subiculum, lateral septum, lateral and basolateral amygdala, bed nucleus of the stria terminalis) and hypothalamus (mediobasal hypothalamus, medial preoptic area and paraventricular nucleus) as well as the nucleus accumbens and mediodorsal thalamus. Intromissions did not contribute significantly to these c-fos changes however. In anoestrus females, exposure to a male only produced a small significant increase in c-fos messenger RNA expression in the temporal cortex inspite of receiving similar amounts of visual and olfactory cues from him and a number of mating attempts. These results clearly demonstrate that changes in sexual motivation markedly alter the neural processing of sensory cues from males. They also show that the hormonal induction of sexual attraction to males cues and the resultant stimulation of sexual behaviour is due not only to altered responsiveness of oestrogen-sensitive brain regions involved in mediating behavioural responses towards the male, but also to changes in primary and secondary/tertiary somatosensory, olfactory and visual processing regions which relay sensory information to them.

Animals↗
PubMed1988

Non-lethal infection of aminergic reticular core neurons: age-dependent spread of ts mutant vesicular stomatitis virus from the nose.

In order to induce a non-lethal infection restricted to central aminergic neurons projecting to the olfactory bulbs a series of temperature sensitive (ts) and G-protein monoclonal antibody escape mutants of vesicular stomatitis virus (VSV) were instilled into the nasal cavity of mice. In three-week (wk)-old NMRI mice four monoclonal antibody escape mutants caused an extensive infection of the olfactory epithelium and, like a wild type strain, a lethal brain infection after spread along olfactory pathways. Three ts mutant strains showed an attenuated pathogenic potential. Strain G31 caused a lethal infection with a somewhat prolonged course while the strain G11 failed to invade the nervous system. Strain G41 showed minimal invasion of central nervous system in three-wk-old mice and caused a lethal infection in newborn and one-wk-old mice. In contrast, two-wk-old mice survived infection with this mutant, which spread along olfactory pathways and rather selectively affected aminergic reticular core neurons in the diagonal band, the locus ceruleus and the raphe nuclei in the brainstem. Thus, an age-dependent virus infection of the olfactory pathways can cause restricted lesions in the brain providing a model for studies of virus-induced changes in aminergic neurotransmission.

Aging↗
PubMed1990

Effect of olfactory bulb ablation on spread of a neurotropic coronavirus into the mouse brain.

Previous results suggested that, after intranasal inoculation, mouse hepatitis virus (MHV), a neurotropic coronavirus, entered the central nervous system (CNS) via the olfactory and trigeminal nerves. To prove this hypothesis, the effect of interruption of the olfactory pathway on spread of the virus was studied using in situ hybridization. Unilateral surgical ablation of this pathway prevented spread of the virus via the olfactory tract on the side of the lesion. MHV RNA could be detected, however, at distal sites on the operated side, indicating that the virus spread via well-described circuits involving the anterior commissure from the control (intact) side of the brain. Viral transport via the trigeminal nerve was not affected by removal of the olfactory bulb, showing that the surgical procedure was specific for the olfactory pathway. These results prove conclusively that MHV gains entry to the CNS via a transneuronal route, and spreads to additional sites in the brain via known neuroanatomic pathways.

Animals↗
PubMed1975

An olfactory projection area in orbitofrontal cortex of the monkey.

An olfactory projection area was studied in monkeys anesthetized with Nembutal. 1. Evoked potentials were recorded when the olfactory bulb (OB) was electrically stimulated in the lateroposterior portion of the orbitofrontal cortex (LPOF). However, those potentials disappeared when the anterior pyriform cortex (AP) (probably together with the medial portion of the amygdala (MA)) was aspirated or electrically destroyed. 2. In nearly the entire hypothalamic region, evoked potentials were recorded by the same stimulation of the OB. When the hypothalamic region was stimulated, evoked potentials were recorded in the LPOF. 3. The evoked potentials in the LPOF due to the OB stimulation never disappeared even when the thalamus was extensively aspirated or destroyed electrically, but they did disappear when the anterolateral and dorsoposterior portions of the hypothalamus were absorbed or electrocoagulated. 4. Evoked potentials in the mediodorsal nucleus (MD) of the thalamus were recorded when the OB was stimulated. When this nucleus was stimulated, evoked potentials were observed in the broad extent of the orbitofrontal cortex anterior to the LPOF, but never in the LPOF itself. 5. Monkeys were conditioned to discriminate two odors. When the LPOF was removed, such ability strikingly decreased; but when other areas in the prefrontal cortex were removed, the ability decreased only slightly. 6. It was concluded that there exists an olfactory pathway from the OB to the LPOF through the AP (and probably the MA) and the hypothalamus, but none through the thalamus, and that the LPOF plays an important role in the discrimination of odors. 7. It was proved that the entorhinal cortex (ER) is neither located as an intermediate olfactory area nor is it situated as a higher area than the LPOF in the newly found olfactory pathway stated above. It may be a link between the high olfactory area and the limbic system.

Animals↗
PubMed2001

Olfactory protocerebral pathways processing sex pheromone and plant odor information in the male moth Agrotis segetum.

We investigated protocerebral processing of behaviorally relevant signals in the turnip moth, Agrotis segetum. Single neurons were studied both physiologically and morphologically using intracellular recording techniques. In moth pheromone communication systems, the presence of the complete, female-produced pheromone blend is necessary for male attraction. We predicted that more protocerebral neurons, compared with AL, would display blend interactions. However, only a few protocerebral neurons responded differently to the blend than could be deduced from the response to single components. The majority of the pheromone-sensitive protocerebral neurons identified in this study responded to the major pheromone component. In coding time, most AL neurons can follow a 5-Hz odor stimulus, whereas most protocerebral neurons failed at higher frequencies than 1 Hz. The majority of neurons that responded to the odorants tested innervated one or both of the protocerebral lateral accessory lobes. If only one of these was innervated, then the innervation always displayed a varicose appearance, suggesting a presynaptic function. Thus, information seems to be transferred from other protocerebral areas to the lateral accessory lobes. Into these, descending neurons sent smooth, postsynaptic branches. A majority of the neurons innervating the superior medial protocerebrum were found to display single-component specificity. Few additional correlations between odor specificity and structural characteristics were apparent.

Animals↗
PubMed1994

Localization and regulation of low affinity nerve growth factor receptor expression in the rat olfactory system during development and regeneration.

Nerve growth factor (NGF), a classic neurotrophic factor, promotes neuronal survival, maintenance, regeneration and differentiation in the peripheral nervous system and parts of the central nervous system. NGF activity is mediated by cell surface bound receptors including the low affinity NGF receptor (LNGFr) which is expressed by some peripheral and central neurons and is present on peripheral nerve Schwann cells during development and regeneration. The olfactory system is a useful model for the study of the role of LNGFr in neuronal development and regeneration. The growth of olfactory axons into the brain begins in the embryo and continues through the first few postnatal weeks. In mature animals there is persistent turnover and generation of olfactory receptor neurons (ORNs) and continuous growth of new axons into the olfactory bulb. These new axons grow along the preexisting olfactory pathway. In the mature olfactory system, LNGFr has been observed in the glomerular layer of the olfactory bulb, the target of ORNs. However, neither the cellular localization nor the developmental expression of LNGFr has been characterized. Here, we tested the hypothesis that LNGFr expression is developmentally regulated in the olfactory nerve and is reinduced following injury to the mature olfactory nerve. LNGFr-immunoreactivity (IR) was first observed in the olfactory mucosa at embryonic day (E)13 and in the olfactory nerve at E14. LNGFr-IR increased in the nerve during embryonic development, began to decrease at around postnatal day (P)5 and was scarcely detectable in normal adults. The staining pattern suggests that LNGFr is located on the olfactory nerve Schwann cells. Streaks of LNGFr-IR were present in the adult olfactory nerve. We reasoned that these streaks might represent transient reexpression of LNGFr associated with normal olfactory neuron turnover and replacement. Consistent with this hypothesis, LNGFr was robustly reexpressed in the adult olfactory nerve following lesion of the olfactory epithelium. Starting late in development (E21) and in the adult, LNGFr-IR was also observed on fibers in deep layers of the olfactory bulb. LNGFr-IR was also observed in neurons of the nucleus of the diagonal band (NDB) in the basal forebrain. NDB is the sole source of cholinergic afferents of the olfactory bulb. Thus, we tested the hypothesis that LNGFr in the deep layers of the olfactory bulb is located on NDB axons by making lesions of NDB. Following the lesion, LNGFr-IR disappeared in the deep layers of the olfactory bulb but remained in the glomerular layer.(ABSTRACT TRUNCATED AT 400 WORDS)

Acetylcholinesterase↗