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PubMed1977

The development of olfactory and hippocampal pathways in the brain of the rat.

The temporal order of development of olfactory, hippocampal and thalamocortical connections has been determined by light microscopy. Scalpel lesions were made to interrupt these connections and the resulting terminal degeneration was stained by Eager's method (1970). A post-operative survival time of one to four days was used. Evidence of the development of these connections was first obtained at the following ages: Olfactory mucosa to olfactory bulb: axon fascicles by 16 days of gestation and terminals in glomeruli at birth; Olfactory bulb to prepyriform cortex at birth; Prepyriform to entorhinal cortex at 13 days after birth; Entorhinal cortex to hippocampus (the perforant path) at 9 days; Hippocampal dentate-Ammonic mossy fibres at 9 days; Hippocampal efferent projection to the septum at birth; Subicular projections to the anterior thalamus at birth and to the mammillary body at 6 days; Hippocampal commissural connections at birth; Corticothalamic and thalamocortical connections by 2 days. These results are discussed in relation to the question of how the development of brain connections is programmed.

Animals↗

PubMed1997

On the protheticity of olfactory pleasantness and intensity.

In Exp. 1, the "protheticity" of the pleasantness of a diverse set of relatively isointensive odorants was estimated using exponents from power functions fitted by an interative least squares procedure between scale values established by (a) magnitude estimation and (b) category rating and rank ordering. In Exp. 2, this procedure was applied to intensity data derived from quarter-log-step volume dilution series of two hedonically disparate odorants, furfural and methyl salicylate. The goodness of fit of the power functions was somewhat better for the intensity than for the pleasantness data. The pleasantness dimension of the diverse stimuli was slightly prothetic (respective category scaling and rank order/magnitude estimation exponents = 0.60 and 0.63). The intensity dimension of furfural was considerably more prothetic than that of methyl salicylate (respective category/magnitude estimation exponents = 0.20 and 0.68; respective rank order/magnitude exponents = 0.21 and 0.69). These data suggest that the degree of olfactory protheticity depends upon the stimuli as well as the attributes chosen for investigation and support the view that Stevens' metathetic/prothetic dichotomy has little utility in classifying the scaling attributes of odors. Whether the degree of protheticity reflects the nature or distribution of olfactory system receptive elements within the main olfactory pathway remains an empirical question which awaits a more specific understanding of the nature of olfactory coding at the level of the neuroepithelium.

Adult↗

PubMed2002

Olfactory transport: a direct route of delivery of inhaled manganese phosphate to the rat brain.

Experiments examining the dosimetry of inhaled manganese generally focus on pulmonary deposition and subsequent delivery of manganese in arterial blood to the brain. Growing evidence suggests that nasal deposition and transport along olfactory neurons represents another route by which inhaled manganese is delivered to certain regions of the rat brain. The purpose of this study was to evaluate the olfactory uptake and direct brain delivery of inhaled manganese phosphate ((54)MnHPO(4)). Male, 8-wk-old, CD rats with either both nostrils patent or the right nostril occluded underwent a single, 90-min, nose-only exposure to a (54)MnHPO(4) aerosol (0.39 mg (54)Mn/m(3); MMAD 1.68 microm, sigma(g) 1.42). The left and right sides of the nose, olfactory pathway, striatum, cerebellum, and rest of the brain were evaluated immediately after the end of the (54)MnHPO(4) exposure and at 1, 2, 4, 8, and 21 d postexposure with gamma spectrometry and autoradiography. Rats with two patent nostrils had equivalent (54)Mn concentrations on both sides of the nose, olfactory bulb, and striatum, while asymmetrical (54)Mn delivery occurred in rats with one occluded nostril. High levels of (54)Mn activity were observed in the olfactory bulb and tubercle on the same side (i.e., ipsilateral) to the open nostril within 1-2 d following (54)MnHPO(4) exposure, while brain and nose samples on the side ipsilateral to the nostril occlusion had negligible levels of (54)Mn activity. Our results demonstrate that the olfactory route contributes to (54)Mn delivery to the rat olfactory bulb and tubercle. However, this pathway does not significantly contribute to striatal (54)Mn concentrations following a single, short-term inhalation exposure to (54)MnHPO(4).

Administration, Inhalation↗

PubMed2004

Oxidative damage in cultured human olfactory neurons from Alzheimer's disease patients.

Oxidative abnormalities precede clinical and pathological manifestations of Alzheimer's disease and are the earliest pathological changes reported in the disease. The olfactory pathways and mucosa also display the pathological features associated with Alzheimer's disease in the brain. Olfactory neurons are unique because they can undergo neurogenesis and are able to be readily maintained in cell culture. In this study, we examined neuronal cell cultures derived from olfactory mucosa of Alzheimer's disease and control patients for oxidative stress responses. Levels of lipid peroxidation (hydroxynonenal), N(epsilon)-(carboxymethyl)lysine (glycoxidative and lipid peroxidation), and oxidative stress response (heme oxygenase-1) were measured immunocytochemically. We found increased levels for all the oxidative stress markers examined in Alzheimer's disease neurons as compared to controls. Interestingly, in one case of Alzheimer's disease, we found hydroxynonenal adducts accumulated in cytoplasmic lysosome-like structures in about 20% of neurons cultured, but not in neurons from control patients. These lysosome-like structures are found in about 100% of the vulnerable neurons in brains of cases of Alzheimer's disease. This study suggests that manifestations of oxidative imbalance in Alzheimer's disease extend to cultured olfactory neurons. Primary culture of human olfactory neurons will be useful in understanding the mechanism of oxidative damage in Alzheimer's disease and can even be utilized in developing therapeutic strategies.

Aldehydes↗

PubMed2002

Mitral cell temporal response patterns evoked by odor mixtures in the rat olfactory bulb.

Mammals generally have the ability to extract odor information contained in complex mixtures of molecular components. However, odor mixture processing has been studied electrophysiologically only in insects, crustaceans, and fish. As a first step toward a better understanding of this processing in high vertebrates, we studied the representation of odor mixtures in the rat olfactory bulb, i.e., the second-order level of the olfactory pathways. We compared the single-unit responses of mitral cells, the main cells of the olfactory bulb, to pure odors and to their binary mixtures. Eighty-six mitral cells were recorded in anesthetized freely breathing rats stimulated with five odorants and their 10 binary mixtures. The spontaneous activity and the odor-evoked responses were characterized by their temporal distribution of activity along the respiratory cycle, i.e., by cycle-triggered histograms. Ninety percent of the mixtures were found to evoke a response when at least one of their two components evoked a response. Mixture-evoked patterns were analyzed to describe the modalities of the combination of patterns evoked by the two components. In most of the cases, the mixture pattern was closely similar to one of the component patterns. This dominance of a component over the other one was related to the responsiveness of the cell to the individual components of the mixture, to the molecular nature of the stimulus, and to the coarse shape of individual response patterns. This suggests that the components of binary mixtures may be encoded simultaneously by different odor-specific temporal distributions of activity.

Acetophenones↗

PubMed2002

Olfactory bulbectomy protects hippocampal pyramidal neurons against excitotoxic death.

The olfactory system is functionally linked to the hippocampus, and odors can modify the activity of hippocampal neurons. Because hippocampal neurons are selectively vulnerable to death in several prominent neurodegenerative conditions, we tested the hypothesis that activity in olfactory pathways can modify the sensitivity of hippocampal neurons to excitotoxic damage. We report that rats subjected to olfactory bulbectomy exhibit a decrease in the vulnerability of hippocampal pyramidal neurons to excitotoxic injury. Four-month-old male Sprague-Dawley rats were subjected to bilateral olfactory bulbectomy or a sham operation. Three months later the rats were given a unilateral infusion of kainic acid in the dorsal hippocampus and were euthanized 24 h later. There was a threefold increase in the number of CA3 neurons that survived kainic acid administration in the bulbectomized rats compared to sham-operated rats. These findings provide the first evidence that olfactory input affects the vulnerability of neurons to excitotoxic death.

Animals↗

PubMed1996

LacZ and OMP are co-expressed during ontogeny and regeneration in olfactory receptor neurons of OMP promoter-lacZ transgenic mice.

The ontogeny and cellular specificity of expression of beta-galactosidase activity and olfactory marker protein (OMP) are compared in olfactory tissue of the H-OMP-lacZ-3 line of transgenic mice. In this line the expression of lacZ is driven by a 0.3 kb fragment of the rat OMP promoter. During fetal development, lacZ expression is detectable in olfactory receptor neurons (ORNs) shortly after the initial appearance of endogenous OMP. The beta-galactosidase marker was observed only in mature olfactory receptor neurons where it co-localized with endogenous OMP. It was absent from immature neurons that express the growth associated phosphoprotein B50/GAP43. Lesion of the peripheral olfactory pathway by intranasal irrigation with Triton X-100 eliminated expression of both OMP and lacZ in the olfactory neuroepithelium. Subsequent regeneration of the full complement of olfactory receptor neurons was associated with co-expression of both OMP and beta-galactosidase activity. Neither OMP nor beta-galactosidase activity was induced in any other cell type of the regenerating olfactory mucosa. Thus, as little as 0.3 kb of the OMP promoter has the ability to target lacZ expression to olfactory receptor neurons in a temporally and spatially defined manner. We discuss the potential utility of this transgenic line for future studies of the olfactory system.

Animals↗

PubMed1995

Brain FOS-like expression in developing and adult honeybees.

This study was undertaken to examine the expression of the protooncogene c-fos in an invertebrate, the honeybee. We investigated first the expression of Fos-like proteins, testing different methodologies (immunohistochemistry, immunocytochemistry, immunoblotting). These studies were carried out at the embryonic, nymphal and adult stages. We found immunoreactive bands at approximately 30 kD and 57 kD. The first ones are revealed at the embryonic, nymphal and adult stages. The approximately 57 kD proteins are present at the adult stage. Beside this qualitative variation, intensive modification occurs with a burst of protein expression a few days after the insect emergence. The results suggest that Fos-like proteins are found in the developing and maturing nervous system. Basal level of expression is found in the olfactory pathway, convincing to explore the protooncogene c-fos expression in the cellular and molecular analyses of olfactory plasticity.

Animals↗

PubMed2004

Olfactory fear conditioning induces field potential potentiation in rat olfactory cortex and amygdala.

The widely used Pavlovian fear-conditioning paradigms used for studying the neurobiology of learning and memory have mainly used auditory cues as conditioned stimuli (CS). The present work assessed the neural network involved in olfactory fear conditioning, using olfactory bulb stimulation-induced field potential signal (EFP) as a marker of plasticity in the olfactory pathway. Training consisted of a single training session including six pairings of an odor CS with a mild foot-shock unconditioned stimulus (US). Twenty-four hours later, the animals were tested for retention of the CS as assessed by the amount of freezing exhibited in the presence of the learned odor. Behavioral data showed that trained animals exhibited a significantly higher level of freezing in response to the CS than control animals. In the same animals, EFPs were recorded in parallel in the anterior piriform cortex (aPC), posterior piriform cortex (pPC), cortical nucleus of the amygdala (CoA), and basolateral nucleus of the amygdala (BLA) following electrical stimulation of the olfactory bulb. Specifically, EFPs recorded before (baseline) and after (during the retention test) training revealed that trained animals exhibited a lasting increase (present before and during presentation of the CS) in EFP amplitude in CoA, which is the first amygdaloid target of olfactory information. In addition, a transient increase was observed in pPC and BLA during presentation of the CS. These data indicate that the olfactory and auditory fear-conditioning neural networks have both similarities and differences, and suggest that the fear-related behaviors in each sensory system may have at least some distinct characteristics.

Amygdala↗

PubMed1989

Recovery of olfactory behavior following removal of accessory olfactory bulb in adult rat.

It has been shown that male rats demonstrate a preference for the odor of the female rat. This preference has been suggested to be a function of the accessory olfactory pathway. Thus, changes in preference of the male rat for the odor of the female were examined following accessory olfactory bulb (AOB) removal. Preference decreased to about 30% of that seen in the intact rat during the 10 days following AOB removal. Thereafter, it increased gradually over one month survival time up to approximately 70% of the level demonstrated by the intact rat. The rats whose main olfactory bulb and AOB were removed did not show any recovery at any survival time. The time course of the behavioral recovery after AOB removal was compared with the time course of the recovery of synaptic density which was observed in the medial amygdaloid nucleus after AOB removal. The relationship between functional recovery and reorganization of synaptic connections is discussed.

Animals↗

PubMedDate not supplied

Physostigmine enhances performance on an odor mixture discrimination test.

Acetylcholine is found within key sectors of the olfactory pathway, and is the neurotransmitter for many bulbopetal axons terminating in the glomerular and internal plexiform layers of the olfactory bulb. The present study determined whether systemically administered physostigmine, a cholinesterase inhibitor, alters the rat's ability to discern among odorant mixtures. Following appropriate training, the performance of eight rats was measured every third day on an odor mixture discrimination test with six levels of difficulty. On each test day (separated from one another by 3 days), a different drug treatment was administered [i.e., 0.00 (saline), 0.05, 0.10, or 0.20 mg/kg physostigmine]. The presentation order of the treatments was counterbalanced across subjects using 4 x 4 Latin squares. The mixture discrimination test consisted of discerning the odor of an airstream coming from the saturated head space of a 1% concentration of ethyl acetate from an airstream saturated with a 1% concentration of ethyl acetate and various concentrations of butanol (i.e., 1, 0.5, 0.1, 0.05, 0.01, or 0.005%). Physostigmine was found to enhance odor discrimination performance on the more difficult discrimination tasks in a dose-related manner, suggesting that cholinergic activation may sharpen the ability of rats to discern subtle differences among complex odor stimuli.

Animals↗

PubMed1995

The effect of anosmia on MK-801-induced behaviour in mice.

Systemic administration of N-methyl-D-aspartate (NMDA) receptor antagonists induces a well defined behaviour in rodents characterized by, for example increased locomotion and ataxia. It is not clear in what brain region(s) NMDA antagonists induce this behaviour. We have studied the possible involvement of olfactory pathways by making adult mice anosmic via intranasal injection of zinc sulphate, a procedure that is known to destroy the olfactory epithelium. The NMDA antagonist MK-801 was given intraperitoneally (0.1-1.0 mg/kg) and the animals were scored for locomotion and ataxia 60-90 min later. Before MK-801 administration, olfactory-lesioned mice did not differ from non-lesioned controls with regard to locomotion or ataxia. MK-801 caused locomotor activation (> or = 0.2 mg/kg) and ataxia (> or = 0.5 mg/kg) in both groups. In general, olfactory-lesioned animals showed more locomotion and less ataxia after MK-801 administration than non-lesioned animals. Lesioned animals displayed 2.0- (P < 0.05) and 3.7-fold (P < 0.05) more extensive locomotor activation than non-lesioned animals after 0.5 and 1.0 mg/kg of MK-801, respectively. No difference in the degree of ataxia was seen between the two groups at 0.5 mg/kg, whereas non-lesioned animals showed a 2.1-fold higher degree of ataxia after 1.0 mg/kg of MK-801, indicating that the enhanced MK-801-induced locomotor activation in olfactory-lesioned mice was not simply due to less ataxia. These results suggest that olfactory input is involved in NMDA antagonist-induced behaviour.

Animals↗

PubMed2002

Bovine herpesvirus 5 (BHV-5) Us9 is essential for BHV-5 neuropathogenesis.

Bovine herpesvirus 5 (BHV-5) is a neurovirulent alphaherpesvirus that causes fatal encephalitis in calves. In a rabbit model, the virus invades the central nervous system (CNS) anterogradely from the olfactory mucosa following intranasal infection. In addition to glycoproteins E and I (gE and gI, respectively), Us9 and its homologue in alphaherpesviruses are necessary for the viral anterograde spread from the presynaptic to postsynaptic neurons. The BHV-5 Us9 gene sequence was determined, and the predicted amino acid sequence of BHV-5 Us9 was compared with the corresponding Us9 sequences of BHV-1.1. Alignment results showed that they share 77% identity and 83% similarity. BHV-5 Us9 peptide-specific antibody recognized a doublet of 17- and 19-kDa protein bands in BHV-5-infected cell lysates and in purified virions. To determine the role of the BHV-5 Us9 gene in BHV-5 neuropathogenesis, a BHV-5 Us9 deletion recombinant was generated and its neurovirulence and neuroinvasive properties were compared with those of a Us9 rescue mutant of BHV-5 in a rabbit model. Following intranasal infection, the Us9 rescue mutant of BHV-5 displayed a wild-type level of neurovirulence and neural spread in the olfactory pathway, but the Us9 deletion mutant of BHV-5 was virtually avirulent and failed to invade the CNS. In the olfactory mucosa containing the olfactory receptor neurons, the Us9 deletion mutant virus replicated with an efficiency similar to that of the Us9 rescue mutant of BHV-5. However, the Us9 deletion mutant virus was not transported to the bulb. Confocal microscopy of the olfactory epithelium detected similar amounts of virus-specific antigens in the cell bodies of olfactory receptor neuron for both the viruses, but only the Us9 rescue mutant viral proteins were detected in the processes of the olfactory receptor neurons. When injected directly into the bulb, both viruses were equally neurovirulent, and they were transported retrogradely to areas connected to the bulb. Taken together, these results indicate that Us9 is essential for the anterograde spread of the virus from the olfactory mucosa to the bulb.

Amino Acid Sequence↗

PubMed1975

[Comparison of the effects of anosmia induced by either peripheral lesion or bulbectomy upon the feeding pattern of the rat (author's transl)].

In order to support the contention that the feeding pattern seen after olfactory bulb removal is due to a sensory loss, the feeding pattern of rats was studied after a peripheral chemical lesion of the olfactory mucosa. A conditioned smell aversion procedure was used to assess the occurence and duration of anosmia after the topical application of zinc sulfate to the olfactory mucosa. It was found that the sensory deficit induced by the peripheral lesion lasted from four to six days. The occurrence of the disrupted feeding pattern in the peripherally lesioned rats coincided in time with the short period of anosmia. Thus, the disruption of the feeding pattern after bulbectomy and after lesions of the central olfactory pathways is clearly the result of anosmia and not of the loss of other non-sensory functions of the olfactory bulbs.

Animals↗

PubMed1999

Coherent oscillations in membrane potential synchronize impulse bursts in central olfactory neurons of the crayfish.

Lateral protocerebral interneurons (LPIs) in the central olfactory pathway of the freshwater crayfish Procambarus clarkii reside within the lateral protocerebrum and receive direct input from projection neurons of the olfactory midbrain. The LPIs exhibit periodic (0.5 Hz) changes in membrane potential that are imposed on them synaptically. Acute surgical experiments indicate that the synaptic activity originates from a group of oscillatory neurons lying within the lateral protocerebrum. Simultaneous intracellular recordings from many LPI pairs indicate that this periodic synaptic input is synchronous and coherent among the population of approximately 200 LPIs on each side of the brain. In many LPIs, specific odors applied to antennules in isolated head preparations generate long-lasting excitatory postsynaptic potentials and impulse bursts. The impulse bursts are generated only near the peaks of the ongoing depolarizations, approximately 1 s after stimulus application, and so the periodic baseline activity is instrumental in timing burst generation. Simultaneous recordings from pairs of LPIs show that, when impulse bursts occur in both cells after an odorant stimulus, they are synchronized by the common periodic depolarizations. We conclude that the common, periodic activity in LPIs can synchronize impulse bursts in subsets of these neurons, possibly generating powerful long-lasting postsynaptic effects in downstream target neurons.

Animals↗

PubMed1984

Herpes simplex encephalitis. Immunohistological demonstration of spread of virus via olfactory and trigeminal pathways after infection of facial skin in mice.

An immunohistological study of viral antigen (VA) in the brain was carried out in mice which had been infected with herpes simplex type 1 virus (HSV) in the skin of the face. In 77% of the mice with VA in the brain the olfactory system as well as the trigeminal system/brainstem was affected. The remaining 23% had VA in the trigeminal system/brainstem only. Eye swab cultures yielded HSV from all mice with VA in the olfactory system. The ease of access of virus infecting the face to the olfactory system shown in this model may have implications for human infections.

Animals↗

PubMed2005

Adenovirus-mediated gene transfer in olfactory epithelium and olfactory bulb: a long-term study.

OBJECTIVES: We sought to study the spatiotemporal gene expression mediated by adenoviral vector in the olfactory pathways. METHODS: The replication-defective adenoviral vector AxCALacZ, which encodes the enzyme Escherichia coli beta-galactosidase, was applied to mouse olfactory epithelium by intranasal instillation. RESULTS: The LacZ gene product, beta-galactosidase, was expressed not only in the olfactory receptor neurons and their axons, but also in the olfactory bulbs. The first evidence of anterograde labeling was observed at postinfection day (PID) 2. At PID 3, beta-galactosidase was strongly expressed in olfactory nerve axons, as well as their terminal glomeruli, in the olfactory bulbs. beta-Galactosidase expression persisted up to PID 90, and there was a significant decrease in the number of labeled neurons at PID 30. CONCLUSIONS: These results suggest possible long-term effects of adenovirus-mediated gene transfer on the olfactory neurons, as well as the olfactory bulbs.

Adenoviridae↗

PubMed1999

[Expression of c-fos prooncogene in rat brain induced by an olfactory stimulus].

OBJECTIVE: In order to investigate how widespread the activated regions induced by an olfactory stimulus throughout the central nervous system (CNS), c-fos expressions in CNS of the rat observed, which is known as a combined morphologically and functionally probe. METHODS: Rats were stimulated by iso-amyl acetate for about 10 times, then one hour later sacrificed with perfusion of fixatives. After ABC immunocytochemi cal staining with anti-c-fos polyclonal antiserum, the c-Fos protein labelling areas on sections of the brain were observed. RESULTS: The results showed that the labelling areas were estremely widespread throughout the brain and cervical segments of the spinal cord in the rat, expecially much more in the areas above the level of the pons. Nearly all neuronal structures in the limbic system were labeled in addition to structures of the olfactory pathways, suggesting there were neuronal activities in multiple neural circuits, which may be associated with emotional, somatic and visceral responses to the olfactory stimulus. Next, many brain areas which were associated with mechanisms of attention and central state regulation were widely labeled. Unexpected heavy labellings in deep layers of the superior colliculus, inferior colliculus and pontine nuclei were presumably relevant to integrating activity between sensations and motions. CONCLUSIONS: The present study indicated that a specific olfactory stimulus did induce widespread activities of so-called pan-brain networks within the central nervous system.

Animals↗