Rhinencephalic structures and their anatomical organization.
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Recent advances in endoscopic evaluation of the nose and paranasal sinuses and endoscopic sinus surgery, coupled with the development of standardized testing of olfactory acuity, have permitted improved correction of olfactory dysfunction. Conversely, increase in the number of operations performed has increased the number of injuries to the olfactory pathways. The mechanisms of loss and potential preventive and corrective measures are reviewed with a goal to minimize the numbers of these complications.
Olfactory transduction is mediated by neuroepithelial cells localized on turbinal crests in naris. Odorant molecules are uptaked by the mucosa which flows on epithelial surface and some of the molecules enter in contact with olfactory cells tentacles. Odorant molecules interact with molecular receptors bound to cell membrane and induced successive reactions leading to ion channels opening and then to receptor potential appearance. The receptor cells degenerate when molecular receptors are saturated and, further regenerate, according a genetic program and olfactory learning action potentials which appear at the basal pole of the receptor cell are propagated along the small olfactory nerves to the olfactory bulb glomerulus. Several hundred axons enter in one glomerulus among others and make synaptic contacts with one dendritic tree of a mitral cell. The selection of the numerous signals which converge in the glomerulus, the codage in intensity, duration and contrast are made at this level. One odorant molecule activates some glomeruli (rarely one); a complex odor activates a great number of glomeruli according a complex spatial distribution. Following odor stimulation, the electrical signals are analysed in the olfactory bulb which delivers to the olfactory cortex various informations about the odor components that are to be selected and compared to anterior olfactory learning. Animal experimentation and clinical data show that memory storage is made using short, medium and long term memorization. This memory is integrated in the limbic system at the interface of neural structures which regulate the main behaviors and physiological functions. This explains the modulatory role of smell in some behaviors but complicate our understanding of access to olfactory memory.
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The anterior olfactory nucleus (AON) is located caudal to the olfactory bulb in the olfactory peduncle. Although this important structure is involved in the bilateral coordination of olfactory information, relatively little is known about its development, structure, or function. The present report details results from an immunohistochemical examination of specific neuronal (microtubule-associated protein-2: MAP2, calbindin D28-k, neuropeptide-Y: NPY) and glial (astrocytes: glial fibrillary-associated protein, or GFAP, oligodendrocytes; RIP) populations in postnatal Days 10, 20, and 30 rats. MAP2-immunoreactivity (-ir), was present throughout the AON, although most dense in the outer plexiform layer. Increases in labeling occurred from Day 10 to Day 30, reflecting the maturation of dendritic processes. Both temporal and regional differences in expression were found with the two neuronal markers. For example, although substantial numbers of calbindin-ir cells were observed as early as Day 10, relatively few cells exhibited NPY-ir. An apparent decline in the number of stained figures was observed from Days 20-30 with both markers. Most cells exhibiting calbindin- or NPY-ir were found in the inner half of the cellular zone of the AON. GFAP-ir was localized mainly to the subependymal zone and the lateral olfactory tract (LOT) at Day 10, with successive increases in staining in the cellular and plexiform layers at Days 20 and 30. Oligodendrocyte-ir was restricted to the anterior commissure and the LOT at Day 10, with dramatic increases in labeling of the cellular and plexiform layers observed by Days 20 and 30. These results represent some of the first analyses of the maturation of specific cellular phenotypes within this large neural region.
Studies of olfaction have focused mainly on neural processing of information about the chemistry of odors, but olfactory stimuli have other properties that also affect central responses and thus influence behavior. In moths, continuous and intermittent stimulation with the same odor evokes two distinct flight behaviors, but the neural basis of this differential response is unknown. Here we show that certain projection neurons (PNs) in the primary olfactory center in the brain give context-dependent responses to a specific odor blend, and these responses are shaped in several ways by a bicuculline-sensitive GABA receptor. Pharmacological dissection of PN responses reveals that bicuculline blocks GABAA-type receptors/chloride channels in PNs, and that these receptors play a critical role in shaping the responses of these glomerular output neurons. The firing patterns of PNs are not odor-specific but are strongly modulated by the temporal pattern of the odor stimulus. Brief repetitive odor pulses evoke fast inhibitory potentials, followed by discrete bursts of action potentials that are phase-locked to the pulses. In contrast, the response to a single prolonged stimulus with the same odor is a series of slow oscillations underlying irregular firing. Bicuculline disrupts the timing of both types of responses, suggesting that GABAA-like receptors underlie both coding mechanisms. These results suggest that glomerular output neurons could use more than one coding scheme to represent a single olfactory stimulus. Moreover, these context-dependent odor responses encode information about both the chemical composition and the temporal pattern of the odor signal. Together with behavioral evidence, these findings suggest that context-dependent odor responses evoke different perceptions in the brain that provide the animal with important information about the spatiotemporal variations that occur in natural odor plumes.
Odorant information is encoded by a series of intracellular signal transduction events thought to be mediated primarily by the second messenger cAMP. We have found a subset of olfactory neurons that express the cGMP-stimulated phosphodiesterase (PDE2) and guanylyl cyclase-D (GC-D), suggesting that cGMP in these neurons also can have an important regulatory function in olfactory signaling. PDE2 and GC-D are both expressed in olfactory cilia where odorant signaling is initiated; however, only PDE2 is expressed in axons. In contrast to most other olfactory neurons, these neurons appear to project to a distinct group of glomeruli in the olfactory bulb that are similar to the subset that have been termed "necklace glomeruli." Furthermore, this subset of neurons are unique in that they do not contain several of the previously identified components of olfactory signal transduction cascades involving cAMP and calcium, including a calcium/calmodulin-dependent PDE (PDE1C2), adenylyl cyclase III, and cAMP-specific PDE (PDE4A). Interestingly, these latter three proteins are expressed in the same neurons; however, their subcellular distribution is distinct. PDE1C2 and adenylyl cyclase III are expressed almost exclusively in the olfactory cilia whereas PDE4A is present only in the cell bodies and axons. These data strongly suggest that selective compartmentalization of different PDEs and cyclases is an important feature for the regulation of signal transduction in olfactory neurons and likely in other neurons as well. In addition, the data implies that an olfactory signal transduction pathway specifically modulated by cGMP is present in some neurons of the olfactory neuroepithelium.
BACKGROUND: Behavioral responses to odorants require neurons of the higher olfactory centers to integrate signals detected by different chemosensory neurons. Recent studies revealed stereotypic arborizations of second-order olfactory neurons from the primary olfactory center to the secondary centers, but how third-order neurons read this odor map remained unknown. RESULTS: Using the Drosophila brain as a model system, we analyzed the connectivity patterns between second-order and third-order olfactory neurons. We first isolated three common projection zones in the two secondary centers, the mushroom body (MB) and the lateral horn (LH). Each zone receives converged information via second-order neurons from particular subgroups of antennal-lobe glomeruli. In the MB, third-order neurons extend their dendrites across various combinations of these zones, and axons of this heterogeneous population of neurons converge in the output region of the MB. In contrast, arborizations of the third-order neurons in the LH are constrained within a zone. Moreover, different zones of the LH are linked with different brain areas and form preferential associations between distinct subsets of antennal-lobe glomeruli and higher brain regions. CONCLUSIONS: MB is known to be an indispensable site for olfactory learning and memory, whereas LH function is reported to be sufficient for mediating direct nonassociative responses to odors. The structural organization of second-order and third-order neurons suggests that MB is capable of integrating a wide range of odorant information across glomeruli, whereas relatively little integration between different subsets of the olfactory signal repertoire is likely to occur in the LH.
Following an olfactory bulb lesion in guinea pig (2 to 3 days), neuronal degeneration occurs in several olfactory-bulb-related areas, primarily in the piriform cortex. The degenerating neurons, which are argyrophilic, are also found in the posterolateral cortical amygdaloid nucleus and the ventrolateral entorhinal cortex. It is suggested that the neurons degenerate because of a transneuronal effect due to a sudden loss of afferent input from the olfactory bulb, although a retrograde effect acting in concert with transneuronal factors cannot be excluded. Terminal degeneration can be identified in several areas outside the olfactory bulb projection area, and is interpreted as degeneration in the axons of the degenerating cortical neurons. Such terminal degeneration, which is best seen 3 to 4 days postoperatively, has been identified in part of the basolateral amygdaloid complex, in the basomedial amygdaloid nucleus, and in the temporal parts of the fascia dentata of the hippocampal formation. Terminal degeneration has also been observed in the deep layers of the anterior olfactory nucleus, the olfactory tubercle, the nucleus of the lateral olfactory tract, and the anterior amygdaloid area. All these projections, apparently, represent the second link in two-neuron pathways, where mitral or tufted cells in the olfactory bulb make up the first neuron. This interpretation was confirmed in control experiments in which areas of argyrophilic neurons coincided with the location of retrogradely labeled neurons following injection of fluorescent substances into several of the above-mentioned areas of terminal degeneration.
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The degree to which maternally derived antibodies may affect neural invasion of Aujeszky's disease virus (ADV) in neonatal pigs was examined. One-week-old pigs with different levels of maternal immunity were inoculated intranasally with 10(7.0) TCID50 of the Ka strain. The invasion of the virus was studied in both the trigeminal neural pathway (nasal mucosa, trigeminal ganglion = 1st level, pons/medulla = 2nd level and cerebellum/thalamus = 3rd level) and the olfactory neural pathway (olfactory mucosa = 1st level, olfactory bulb = 2nd level and lateral olfactory gyrus = 3rd level) by virus titration and immunohistochemistry (IHC). In control pigs without specific antibodies, virus invaded all neuronal levels in both neural pathways. In pigs with a low concentration of maternal antibodies (SN-titer = 2-3), virus infected all neuronal levels in both neural pathways but, compared to the controls, virus titers were significantly lower (approximately 2 log10) in the trigeminal pathway. In pigs with a high concentration of maternal antibodies (SN-titer = 272-384), virus reached the 2nd neuronal level of the olfactory pathway while no neural tissue had been infected in the trigeminal pathway. Virus titers in the affected neuronal levels of the latter pigs were significantly lower than in the controls. IHC revealed, in non-immune pigs, a fibroblast-mediated spread of the virus in the nasal lamina propria, and a local spread of the virus from neurons to their satellite cells in the trigeminal ganglion. Such a spread of the virus was rarely seen in the nasal mucosa and in the trigeminal ganglion of passively immune pigs. These findings suggest that, in the presence of maternal immunity, defence mechanisms operate at these sites. In conclusion, we can state that a correlation exists between the level of maternal immunity and the protection against invasion of ADV in the nervous system of neonatal pigs.