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PubMed1997

Phorate-induced enzymological alterations in mouse olfactory bulb.

The organophosphate pesticide, phorate, is an extremely hazardous insecticide. Not much experimental study is available on effects of phorate on different brain areas. We report in this study the alterations induced by phorate on enzyme profile of mouse olfactory bulb. Olfactory bulb, the first processing centre after the sensory cells in the olfactory pathway, has connections with the other higher centres of the brain like hippocampus and hypothalamus. Phorate was administered orally in the diet at the doses of 1.0 mg and 1.5 mg/kg body weight to adult albino mice. After 32 weeks of exposure animals were sacrificed and cryosections were processed for acetylcholinesterase and butyrylcholinesterase (AChE and BChE, respectively) enzyme localization. Significant reduction occurs in AChE and BChE activity at higher dose level, whereas reduced BChE activity was found at both dose levels. Our results shows an obvious effect on cholinesterase enzyme profile of olfactory bulb of mice after systemic administration of low doses of phorate for long terms.

Acetylcholinesterase↗
PubMed1983

3H-thymidine-radiographic studies of neurogenesis in the rat olfactory bulb.

Neurogenesis in the rat olfactory bulb was examined with 3H-thymidine-radiography. For the animals in the prenatal groups, the initial 3H-thymidine exposures were separated by 24 h; they were the offspring of pregnant females given two injections on consecutive embryonic (E) days (E12-E13, E13-E14, . . . E21-E22). For the animals in the postnatal (P) groups, the initial 3H-thymidine injections were separated by 48 h, each group receiving either four (PO-P3, P2-P4, . . . P6-P9) or two (P8-P9, P10-P11, . . . P20-P21) consecutive daily injections. On P60, the percentage of labeled cells and the proportion of cells added during either 24 h or 48 h periods were quantified at several anatomical levels for each neuronal population in the main olfactory bulb (mitral cells, tufted cells, granule cells, interneurons in the external plexiform layer, periglomerular granule cells) and accessory olfactory bulb (output neurons, granule cells, periglomerular granule cells). The total time span of neurogenesis extends from E12 to beyond P20. Output neurons are prenatally generated over 5-9 day periods (with most neurogenesis occurring over 2-4 days) in a strict sequential order beginning with the accessory bulb output neurons (E13-E14) and ending with the interstitial tufted cells lying between the glomeruli in the main bulb (E20-E22). These data are correlated with the main and accessory bulb projection fields in the amygdala and with the chronology of amygdala neurogenesis. With the exception of the granule cells in the accessory bulb (88% generated between E15-E22), the rest of the interneuronal populations are generated postnatally and nearly simultaneously. While most neurons (75-80%) originate during the first three weeks of life, all interneuronal populations, including accessory bulb granule cells, show some neurogenesis beyond P20. Injections of 3H-thymidine in juvenile and adult rats indicates neurogenesis up to P60 in the accessory bulb and up to P180 in the main bulb, especially in the main bulb granule cell population. There is circumstantial evidence for turnover of main bulb granule cells during adult life.

Animals↗
PubMed1997

Odor exposure reveals non-uniform expression profiles of c-Jun protein in rat olfactory bulb neurons.

In the main olfactory bulb, neurons are arranged strategically in distinct layers among which translaminar synaptic transmission can be made from the superficial, sensory to the deep, output layers that account for the processing of olfactory information. To search for stimulus-transcription coupling thought to be operated differentially in several cell types, c-Jun expression was examined immunohistochemically in rat olfactory bulb following 30-min odor stimulation with acetic acid and 1-butanol. c-Jun was rapidly induced in neuronal cell nuclei belonging to periglomerular, tufted, mitral and granule cells. The disappearance of c-Jun, however, differed between each cell type. In the glomerular layer, the glomeruli composed of c-Jun-expressing periglomerular cells were seen. Different odors led to labeling of different sets of glomeruli. The labeled periglomerular cells disappeared within 2 h. In all the deeper layers, however, a rather homogeneous label was noted for the tufted, mitral and granule cells present throughout the olfactory bulb, regardless of the difference in odor. In tufted and mitral cells, the c-Jun expression persisted for 4 days after odor stimulation. In the granule cell layer, numerous granule cells increased c-Jun immunoreactivity which lasted for 1 day following odor application. In control rats which were given clean air, the basal amount of c-Jun expression was seen confined to scattered granule cells. The results suggest that c-Jun is expressed in a variety of odorant-stimulated bulb neurons with a time course being dependent on cell type.

1-Butanol↗
PubMed1994

Synaptology of cultured olfactory bulb cells.

Cultured embryonic mouse olfactory bulb cells formed asymmetric, symmetric, axodendritic, and dendrodendritic synapses. These neurons contained electron lucent, dense core, and coated vesicles. Dense core and coated vesicles had an average diameter of 71 and 80 nm, respectively. Two statistically different populations of electron lucent vesicles were found, based on synaptic symmetry: electron lucent vesicles from asymmetric synapses had an average diameter of 46 nm with an estimated volume of 49,000 nm3, whereas those from symmetric synapses had an average diameter of 44 nm and an estimated volume of 42,000 nm3. Because these values are similar to those found for intact olfactory bulb, the synapses of these cultured cells have some of the same morphological characteristics as those in the intact olfactory bulb.

Animals↗
PubMed1996

The structural localization of galanin, and its function in modulating acetylcholine release in the olfactory bulb of adult rat.

The localization of galanin immunoreactivity was analyzed within the olfactory bulb of adult rats. Galanin-positive neurons were differentially distributed among the bulb layers. The density of stained neurons was highest in the glomerular and external plexiform layers. According to morphology, size, location and arrangement, a large proportion of galanin-immunoreactive neurons corresponds to external tufted cells and short-axon neurons in the superficial part of the external plexiform and glomerular layers. A smaller number were middle tufted cells and short-axons neurons while only a few short-axon neurons were labeled in the granule cell layer. Galanin-stained nerve fibers had different structures (thick fibers with or without varicosities, and thin fibers with or without varicosities). Among them were afferent immunoreactive nerve fibers entering the bulb through the olfactory nerve layer, but penetrating superficial layers. Correspondingly, a large number of galanin-positive axons (with or without varicosities) were observed in the olfactory nerve layer. A number of galanin-positive nerve fibers was also present in the glomerular and internal plexiform layers, while these fibers were scarce in the granule cell layer, their density was lowest in the external plexiform layer. These results suggest that galanin-positive axons present in the olfactory bulb originate from at least four different sources. From the periphery axon bundles enter the bulb together with olfactory nerve fibers from the rostral direction and with a fiber bundle from the ventral posterior surface, i.e. at the border between the olfactory tract and the main olfactory bulb along a large blood vessel. Central sources are local interneurons in the olfactory bulb and some extrabulbar brain regions. Double-labeling experiments combining acetylcholinesterase histochemistry with galanin immunocytochemistry did not show any co-localization of acetylcholinesterase and galanin in nerve cell perikarya or nerve fibers. Synthetic porcine galanin (1-29) promoted acetylcholine release in olfactory bulb tissue slices, suggesting that galanin can effectively modulate cholinergic transmission and perhaps other forms of neuronal transmission. It is concluded that galanin may be significantly involved in olfactory processing at cellular and synaptic levels.

Acetylcholine↗
PubMed2002

Lateral inhibition in the olfactory bulb and in olfaction.

Lateral inhibition in the olfactory bulb is mediated by circuits that involve reciprocal dendrodendritic connections between mitral and granule cells. Because of the properties of these connections and also because odor stimuli are not represented in an obviously topographic fashion, questions have been raised about whether the function of local inhibition in the olfactory bulb can be compared to the function of inhibition in other brain areas. Here, I propose an analysis of local inhibition in the olfactory bulb based on the simplification that olfactory bulb circuitry can be thought of as implementing a simple linear two-dimensional filter. This analysis highlights some important characteristics of the circuitry of the olfactory bulb and suggests that the function of lateral inhibition in the olfactory bulb may be to compensate for generalized, spatially distributed activation that otherwise may obscure the specific, discrete patterns of glomerular activation seen across the olfactory bulb.

Animals↗
PubMed2003

Organization of postsynaptic density proteins and glutamate receptors in axodendritic and dendrodendritic synapses of the rat olfactory bulb.

Glutamate neurotransmission in the olfactory bulb involves both axodendritic synapses and dendrodendritic reciprocal synapses and possibly also extrasynaptic receptors. By using a sensitive immunogold procedure, we have investigated the organization of two synaptic scaffolding molecules, PSD-95 and PSD-93, as well as N-methyl-D-aspartate (NMDA) and alpha-amino-3-hydroxy-5-methylisoxazole-4-proprionic acid (AMPA) receptors, at these heterogeneous glutamate signaling sites. Immunolabeling for PSD-95 and PSD-93 was present in all major types of putative glutamatergic synapse, suggesting that these proteins are essential components of the synaptic signaling apparatus. The linear density and the subsynaptic distribution of PSD-95/PSD-93 gold particles did not differ significantly between axodendritic and dendrodendritic synapses. Antibodies recognizing NMDA and AMPA receptor subunits also labeled asymmetric synapses throughout the olfactory bulb. Immunolabeling for the AMPA receptor subunits GluR2/3 was similar in all types of synapse. In contrast, immunogold signals for the NR1 subunit of NMDA receptors varied significantly among different synapse populations, with olfactory nerve synapses in the glomerular layer showing the lowest labeling intensity. Although the lateral dendrites of mitral and tufted cells have been reported to respond to glutamate, they did not display significant plasma membrane labeling for the NR1 subunit or for PSD-95, suggesting that the physiological effects of glutamate at these sites are mediated by NMDA autoreceptors that are not clustered and occur only at a low density on the dendritic surface. Our quantitative analysis of olfactory bulb synapses indicates that the density of NMDA receptors is not determined by the complement of PSD-95/PSD-93. The latter molecules appear to be expressed in an all-or-none fashion and may form a standard lattice common to different types of glutamatergic synapse.

Animals↗
PubMed1993

Differential OMP expression in opossum accessory olfactory bulb.

Using immunohistochemical techniques, olfactory marker protein (OMP) was localized to the main (MOB) and accessory (AOB) olfactory bulbs of 30- and 45-day-old, and adult Brazilian opossums, Monodelphis domestica. Entire olfactory nerve and glomerular layers of the adult opossum MOB were darkly stained. In the adult AOB the rostral half of these two layers was stained more intensely than the caudal half, and both parts were less darkly stained than the MOB. This differential AOB staining was not present at 30 days of age, but was evident by postnatal day 45, although not as dramatic as in adults. This is the first report of differential OMP expression and may provide an approach to identifying the function of OMP.

Aging↗
PubMed2003

Distribution of GluR1 is altered in the olfactory bulb following neonatal naris occlusion.

The olfactory system is well suited for studies of glutamate receptor plasticity. The sensory neurons are glutamatergic, and they turn over throughout life, and the olfactory bulb neurons that process their inputs express many of the known glutamate receptor subunits. Neonatal naris occlusion alters olfactory bulb development and the expression of certain neuroactive substances and receptors, at least in part due to loss of the sensory inputs. We therefore postulated that neonatal naris occlusion might alter glutamate receptor expression during postnatal development. Single nares of newborn mice were occluded on postnatal days 1-2, and the distribution of glutamate receptor subunits was evaluated using immunoperoxidase methods. Light microscopic examination on postnatal day 6 failed to reveal adult-like staining of neuronal cell bodies in the olfactory bulbs. By day 12, cell bodies that were immunoreactive (-IR) for the GluR1 subunit were visible in the external plexiform layer (EPL) of both sides. By day 18, many of the GluR1-IR cell bodies could be identified as cell types that had previously been reported to express homomeric GluR1 receptors. Analysis of single, mid-dorsal sections from 18-25-day-old mice showed that the medial EPL of the occluded side had a significantly lower density of these cell bodies. The GluR1 staining of the adjacent mitral cell layer (MCL) was also heavier on the occluded side, but no gross differences in staining for other glutamate receptor subunits were observed. Neonatal naris occlusion therefore appears to provide a new model for studying expression of GluR1 receptors during the development of a discrete population of olfactory bulb neurons.

Animals↗
PubMed1990

A histopathological study on senile changes in the human olfactory bulb.

Senile changes in the human olfactory bulb were studied histopathologically in 133 individuals ranging in age from 40 to 91 years with a mean age of 64.3 years. Neurofibrillary tangles (NFTs) in the olfactory bulb were observed in 47 subjects aged over 50 years. The frequency of NFTs was 35.3% (47/133) in total and 40.5% (47/116) among subjects 50 years of age or older. The frequency of individuals with NFTs increased linearly with age. Senile plaques (SPs) were observed in 5 individuals over 60 years old at a frequency of 3.8% (5/133) in total and 5.7% (5/88) among individuals 60 years old or more. Granulovacuolar degeneration was rarely seen, and amyloid angiopathy was not recognized. Senile changes in the hippocampus and parahippocampal gyrus were also examined. In some cases, the frequencies of NFTs and SPs in the hippocampal region were not identical to those in the olfactory bulb. However, it was not apparent whether senile changes first appear in the olfactory bulb or in the hippocampal region.

Adult↗
PubMed1987

Golgi analyses of dendritic organization among denervated olfactory bulb granule cells.

In the vertebrate olfactory bulb, the primary projection neurons, mitral and tufted cells, have reciprocal dendrodendritic synapses with respective subpopulations of anaxonic interneurons called granule cells. In the neurological murine mutant Purkinje Cell Degeneration (PCD), all mitral cells are lost during early adulthood. As a consequence, a subpopulation of granule cells is deprived of both afferent input and efferent targets. The effect of this event on the morphology and sublaminar distribution of granule cells was studied with light microscopic Golgi procedures in affected homozygous recessive PCD mutants and normal heterozygous littermate controls. In the control mice, a minimum of three subpopulations were identified predominantly on the basis of the topology of apical dendrites and their spinous processes within the external plexiform layer (EPL) of the olfactory bulb: type I had dendrites extending across the full width of the EPL and a homogeneous distribution of spines; type II had dendritic arbors confined to the deeper EPL; type III had apical dendrites that arborized extensively within the superficial EPL with no arbors or spines present in the deeper EPL. Prior studies suggest that type II cells form connections with mitral cells; type III cells form connections with tufted cells; and type I cells may integrate information from both populations of projection neurons. In the mutant PCD mice, the classification of subpopulations of granule cells proved difficult due to a compression of dendritic arbors within the EPL. Dendritic processes followed a more horizontal tangent relative to the radial orientation seen in control mice. The length of dendritic branches was reduced by approximately 20% with a corresponding decrease in the number of spines. The density of spines (#/1 micron of dendrite) was constant in both controls and mutants at approximately 0.21. Truncation of the dendrites in the PCD mutants appeared to occur at terminal portions because the number of dendritic bifurcations was equal in both groups of mice. The data are discussed in terms of subpopulations of granule cells in the mouse olfactory bulb, the sublaminar organization of olfactory bulb circuits, and the capacity for survival and plasticity in the reciprocal dendrodendritic circuits mediated by the granule cell spines.

Animals↗
PubMed1998

[Calretinin immunoreactivity in olfactory bulb and mucosa in mice].

The vertebrate olfactory system is capable of recognizing and discriminating thousands of different odorant molecules. In vitro biochemical studies have shown that some odorants elicit an increase in the intercellular second messenger cyclic AMP, whereas other odorants cause an increase in the second messenger inositol triphosphate (IP3). If IP3 plays an important role in the signal transduction, calcium-binding protein will be needed. We investigated the expression of calretinin, which belongs to the E-F hand family, in the neonatal and adult olfactory mucosa and olfactory bulb. Mice were sacrificed on postnatal day 1 (P1), day 3 (P3), day 10 (P10) and 12 weeks as adults. The olfactory mucosa of the nasal septum and the olfactory bulb were stained with anti-calretinin antibody at a 1:1000 dilution for 48 hours. The results were as follows. 1) Olfactory mucosa: In the P1 mouse, the olfactory nerves running in the submucosal layer and olfactory cells in the epithelium were positive. In the epithelium, immunopositive spots were seen exclusively in the upper half of the epithelium. In the P3, P10 and adult mice, these spots were seen throughout the olfactory cell layer. However, the basal cell layer and supporting cells were negative. 2) Olfactory bulb: In all stages, the olfactory nerve layer and the glomerular layer were strongly stained. In the external plexiform layer, many cells were positive. Their shape was bipolar and the size of the cell body was thought to be about 20 microns. They were thought to be tufted cells. However, there is a possibility that these cells are short axon cells in the external plexiform layer. In the granule layer, some granule cells were positive. In the P1 mouse, the immunopositive spots were exclusively seen in the upper half of the epithelium. In contrast, in the P3 mouse, these spots were seen throughout the olfactory cell layer. Judging from our results, it is suspected that the important change in neurogenesis of olfactory cells occurred between P1 and P3. In the olfactory bulb, from P1 to adult mice, calretinin was positive in the olfactory nerve layer, the glomerulus and periglomerular cells. In contrast, mitral cells were negative. Most reports state that calcium binding protein appears in periglomerular cells. However, in the external plexiform layer, many cells were positive. As their shape was bipolar and the cell body was a little larger than the periglomerular cells, these cells were thought to be tufted cells.

Animals↗
PubMed2002

Origin and migration of interneurons of the olfactory bulb in the musk shrew, Suncus murinus.

The olfactory bulb of the musk shrew, Suncus murinus, is characterized by the presence of various interneurons. Our previous report (Kakuta et al., 2001) demonstrated that positive immunoreactions for calretinin were observed in periglomerular and perinidal cells in the glomerular layer, small ovoid neurons in the external plexiform layer, and granule cells in the granule cell layer of the olfactory bulb in the musk shrew aged 1 to 5 weeks, in addition to calretinin-immunoreactive bipolar cells distributed in the anterior subependymal layer and in each layer of the olfactory bulb. To examine the origin and migration of interneurons of the olfactory bulb, we labeled generated cells by injecting 28-day-old musk shrews with 5-bromo-2'-deoxyuridine (BrdU), and detected the labeled progeny cells that survived after several intervals. BrdU-labeled cells originated in the subependymal layer around the anterior horn of the lateral ventricle, and rostrally migrated in the subependymal layer from the anterior wall of the lateral ventricle into the center of the olfactory bulb, where they radially migrated into the granule cell layer, external plexiform layer, and glomerular layer. It took 2 days to migrate rostrally in the subependymal layer from the anterior lateral ventricle to the center of the olfactory bulb, and 2 to 6 days to migrate radially from the bulbar subependymal layer into the three layers mentioned. The rate of rostralward migration of the labeled cells was estimated to be 38 microm/h, while that of radial migration, 7 to 25 microm/h. The present BrdU-labeling study, together with our previous immunohistochemical study (Kakuta et al., 2001), indicates that anterior subependymal cells differentiate into granule cells in the granule cell layer, into Van Gehuchten cells in the external plexiform layer, and into periglomerular and perinidal cells in the glomerular layer of the olfactory bulb in the musk shrew.

Animals↗
PubMed1997

Olfactory bulb recovery after early sensory deprivation.

Olfactory bulbs retain the ability to acquire new neurons throughout life. Unilateral olfactory deprivation during the first postnatal month in rats results in a dramatic reduction in the size of the experimental olfactory bulb. Part of this reduction is attributable to the death of neurons and glia. To examine the regenerative capacity of the juvenile olfactory bulb, we developed a technique for reversible olfactory deprivation. Reversible blockade from postnatal day 1 (P1) to P20 or P30 results in reduced bulb volume and tyrosine hydroxylase immunostaining, and decreased depth in the olfactory mucosa. In another experiment, normal stimulation was restored for varying periods of time, and experimental and control bulb volumes were measured. Recovery of bulb size occurs after 40 d of normal stimulation. Rats injected with a thymidine analog to label dividing cells during the recovery period revealed that rescue results at least in part from the addition of new neurons and glia. Thus, cells born after the return of normal levels of environmental stimulation can replace some of the neurons and glia that are lost during olfactory deprivation. This system can be used to study mechanisms that underlie neuronal regeneration in the maturing mammalian brain.

Animals↗
PubMed1995

Connections of the olfactory bulb in the chinook salmon (Oncorhynchus tshawytscha).

This report describes the connections of the olfactory bulb in juvenile chinook salmon (Oncorhynchus tshawytscha) as revealed by the retrograde and anterograde transport of biotinylated dextran amine (BDA). Pressure injections of BDA to discrete locations within the bulb reveal that the olfactory bulb projects via medial and lateral tracts to various regions of the dorsal and ventral telencephalon as well as to the diencephalon. Terminal-like boutons are present in the ventral, dorsal, lateral and supracommissural nuclei of the ventral telencephalon and in the lateral-ventral and posterior zones of the dorsal telencephalon. There is also a projection to the nucleus taenia and to the contralateral olfactory bulb. A diencephalic terminal field occurs in the posterior tuberal region of the ventral diencephalon. Olfactory bulb fibers in the preoptic region have axonal varicosities near neurons containing releasing hormones. A synaptic connection is suggested allowing for the possibility that output from the olfactory bulb may directly modulate the activity of these neurons. Telencephalic injections of BDA are used to determine the origins of olfactory bulb efferents. Neurons are retrogradely labeled by BDA in a Golgi-like manner, allowing one to visualize the morphology of olfactory bulb efferents. Three types of neurons in the bulb are filled by injections into the posterior zone of the dorsal telencephalon: mitral cells and ruffed cells in the external cellular layer, and neurons in the internal cellular layer. Although it has been known that both mitral cells and neurons in the internal cellular layer project out of the bulb in teleosts, the use of BDA allowed for an accurate description of the morphology of these extrinsically projecting neurons. This is the first evidence that the ruffed cells in salmon project out of the bulb. The results of this study suggest that the secondary olfactory projections in chinook salmon are consistent with those in other teleosts with minor variations. The data also show that olfactory bulb efferents originate not solely from mitral cells in the external cellular layer but also from ruffed cells in the external cellular layer and neurons in the internal cellular layer. It is proposed that the extrinsically projecting neurons in the internal cellular layer constitute an anterior olfactory nucleus in salmon.

Animals↗
PubMed1994

Noradrenergic modulation of synaptic transmission between olfactory bulb neurons in culture: implications to olfactory learning.

Noradrenergic modulation of the glutamatergic-GABAergic synapses between mitral/tufted (M/T) and granule cells has been implicated in some forms of olfactory learning (5), but the mechanism of action is unknown. Intracellular stimulation of M/T cells in primary culture, evoked glutamate-mediated excitatory postsynaptic potentials (EPSPs) in granule cells that were reversibly inhibited by approximately 50% during application of norepinephrine (NE). NE had no effect, however, on the membrane current evoked by the application of glutamate, indicating a presynaptic site of action. The effect of NE on EPSPs was mimicked by the alpha receptor agonist clonidine, but not by the beta receptor agonist isoproteronol. NE also inhibited spontaneous GABAergic inhibitory postsynaptic potentials recorded in M/T cells, by a presynaptic alpha-adrenergic mediated mechanism. NE and clonidine also inhibited high threshold calcium currents. The effects of NE on calcium currents were irreversible in the presence of internal GTP gamma S and prevented by pertussis toxin, suggesting a G protein-coupled mechanism. Pertussis toxin also prevented the effects of NE on synaptic transmission. These results support previous results suggesting a disinhibitory role for NE in the olfactory bulb. This action is, at least in part, due to a reduction in mitral cell mediated granule cell excitation through inhibition of presynaptic calcium influx.

Animals↗
PubMed1990

Specific binding of insulin to membranes from dendrodendritic synaptosomes of rat olfactory bulb.

The external plexiform layer of the olfactory bulb is among the brain regions where insulin receptors are most abundant. In vitro binding of porcine 125I-insulin to membranes of dendrodendritic synaptosomes isolated from adult rat olfactory bulbs was studied to test the hypothesis that dendrodendritic synapses are major insulin-receptive sites in the external plexiform layer of olfactory bulbs. Of the specific insulin binding sites present in a total particulate fraction from the olfactory bulbs, approximately half were recovered in the dendrodendritic synaptosome fraction. The only other subcellular fraction to which substantial insulin binding was observed was the conventional (axodendritic/axosomatic) synaptosome fraction. Analysis of equilibrium binding of insulin to dendrodendritic synaptosomal membranes, at total insulin concentrations of 0.5-1,000 nM, revealed binding site heterogeneity consistent with a two-site model for insulin binding to a high-affinity (KD = 6 nM), low-capacity (Bmax = 110 fmol/mg of protein) site and a low-affinity (KD = 190 nM), high-capacity (Bmax = 570 fmol/mg of protein) site. The results indicate that the intense labeling of the external plexiform layer of the olfactory bulb in autoradiographic studies of insulin binding can be attributed to insulin receptors on dendrodendritic synaptic membranes in this region.

Animals↗