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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↗
PubMed2005

The alpha6 integrin subunit in the developing mouse olfactory bulb.

Integrins are heterodimeric cell surface receptors that mediate developmental events by binding extracellular matrix ligands. Several lines of evidence suggest a role for integrins, specifically the alpha 6 subunit, in neuronal migration, neurite outgrowth, and axon guidance during olfactory development. Therefore, we undertook an analysis of the expression of the alpha 6 subunit in the olfactory system of the embryonic and early postnatal mouse to understand the role it may play during neural development. In addition, as a functional assay we examined the developmental effects of the loss of this subunit on olfactory development by analyzing an alpha 6 knockout (alpha 6-/-). Immunohistochemical analyses and confocal microscopy were used to examine alpha 6 expression in the CD-1 embryonic and early postnatal olfactory system and also to examine the organization of the olfactory system in the alpha 6-/- mouse. In CD-1 mice from E13 to E17, alpha 6 localizes in radial patterns extending from the core of the olfactory bulb to the nerve layer and colocalizes with RC2, an antibody specific for radial glia. By the day of birth (P0; approximately E19), expression is limited to the external plexiform layer and the olfactory nerve layer, where it colocalizes with laminin and p75. In the alpha 6-/- mouse, areas of ectopic granule cells were observed in the mitral cell layer of the olfactory bulb. These ectopias coincided with areas of disorganization of the radial glial processes and breaks in the mitral cell layer. These observations suggest a role for alpha 6 integrin in neural migration during olfactory development, likely secondary to organization of the radial glial scaffold.

Animals↗
PubMed1993

Experimental evidence for an early commitment of gonadotropin-releasing hormone neurons, with special regard to their origin from the ectoderm of nasal cavity presumptive territory.

The origin and the migration of gonadotropin-releasing hormone (GnRH)-producing neurons were studied using the indirect immunoperoxidase method in normal and surgically operated chick embryos. In normal embryos, during early embryonic development, GnRH neurons were located only in the respiratory and the olfactory epithelia. Then, these neurons followed the nearest nerve bundle and occupied, thereafter, the dorsal, medial or ventral part of the olfactory nerve according to the time and area of the olfactory epithelium they emerged from. At the junction with the forebrain, the majority of GnRH neurons passed ventromedially round the olfactory bulb. Therefore, they penetrated through the interhemispheric space and coursed obliquely toward caudal and dorsal telencephalon from where they will be later distributed to reach their adult-like position. In view of the large distribution of these neurons in the nasal region, unilateral surgical ablation either of the whole or of each presumptive territory of nasal structures was performed from 2 to 4 somite stages. As expected, when both olfactory placode and ectoderm of nasal cavity presumptive territories were unilaterally removed, olfactory nerve, nasal structures and GnRH neurons failed to develop in the operated side. After the unilateral removal of the olfactory placode anlage, the distribution pattern of GnRH neurons was not disturbed in the operated as well as in the control side although ipsilateral olfactory structures were greatly reduced. In contrast, when the presumptive ectoderm of nasal cavity was unilaterally removed, GnRH neurons were detected only in the control side where this territory was left intact. Therefore, from early neurogenesis, GnRH neurons seem to be already committed, and they originate from the ectoderm of nasal cavity presumptive territory.

Animals↗
PubMed1997

Increase of ciliary neurotrophic factor (CNTF) in the ischemic rat brain as determined by a sensitive enzyme-linked immunoassay.

To study the distribution of ciliary neurotrophic factor (CNTF) in the rat brain under physiological as well as pathological conditions, a sensitive sandwich enzyme linked immunoassay (EIA) for rat CNTF was developed using rabbit anti-CNTF antibody. This method detected as little as 10 pg ml-1 CNTF with a good linearity and accuracy. Analysis of various regions of rat brain and peripheral nerves showed a high content of CNTF in the sciatic nerves, spinal cord, optic nerves, and olfactory bulb. Transient focal ischemia of rat brain caused by middle cerebral artery occlusion significantly and specifically increased CNTF levels in the cerebral cortex and hippocampus regions in the ischemic hemisphere.

Animals↗
PubMed1999

TrkA expression in olfactory epithelium and bulb during development.

The purpose of the present study was to examine immunohistochemically the expression of high-affinity nerve growth factor receptor (trkA) in the olfactory nervous system of developing mice and of colchicine-treated adult mice. Olfactory epithelia of embryos and neonates showed trkA immunoreactivity not only in basal cells but in receptor cells, with trkA-immunoreactive olfactory nerve fibers in the subepithelium and the bulb. In adults, trkA immunoreactivity was found only in basal cells of olfactory epithelia. Olfactory epithelia of colchicine-treated adult mice, however, exhibited appearance of trkA-immunoreactive receptor cells and increased trkA immunoreactivity in olfactory nerve fibers. These findings indicate that expression of trkA continually occurs in the olfactory nervous system during life and that trkA can be highly expressed during development.

Animals↗
PubMed2007

Afferent input modulates the chronic hypercapnia-induced increase in respiratory-related central pH/CO2 chemosensitivity in the cane toad (Bufo marinus).

The goal of this study was to examine the role of respiratory-related afferent input on the chronic hypercapnia (CHC)-induced increase in central respiratory-related pH/CO2 chemosensitivity in cane toads (Bufo marinus). Toads were exposed to CHC (3.5% CO2) for 10 days, following which in vitro brainstem-spinal cord preparations were used to assess central respiratory-related pH/CO2 chemosensitivity. Motor output from the vagus nerve root was used as an index of breathing (fictive breathing). Olfactory denervation (OD), prior to exposure to CHC, was used to remove the influence of CO2-sensitive olfactory chemoreceptors, which inhibit breathing. Exposure to chronic hyperoxic hypercapnia (CHH) was used to reduce the level of arterial chemoreceptor input compared with CHC alone. In vivo experiments examined the effects of CHC, CHH and OD on the acute hypercapnic ventilatory response of intact animals. In vitro, a reduction in artifical cerebral spinal fluid (aCSF) pH increased fictive breathing in preparations taken from control and CHC animals. CHC caused an increase in fictive breathing compared with controls. OD and CHH abolished the CHC-induced augmentation of fictive breathing. In vivo, CHC did not cause an augmentation of the acute hypercapnic ventilatory response. CHH reduced the in vivo acute hypercapnic ventilatory response compared with animals exposed to CHC. In vivo, OD reduced breathing frequency and increased breath amplitude in both control and CHC animals. The results suggest that afferent input from olfactory and arterial chemoreceptors, during CHC, is involved in triggering the CHC-induced increase in central respiratory-related pH/CO2 chemosensitivity.

Analysis of Variance↗
PubMed1986

Olfaction.

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Cranial Nerve Diseases↗
PubMed1983

[Neural control of saliva secretion. Review of questions on special neurosecretory functions of the facial nerve].

Fifty years ago, anatomists and physiologists still held the opinion that the N. facialis had a purely motor fuction without any sensory or secretory components. With respect to the previously only occasionally mentioned possibility of an additional neurosecretory function of the N. facialis, clinical and experimental, especially neurophysiological research and experiences of the last five decades have however led to results which are being discussed under particular consideration of the neural control of salivary secretion. In this connection, side-functions are discussed that are just appearing in outlines and have not yet been fully cleared up, for example questions regarding an internal secretion of certain parts of the facial nerve, especially related to the patotid gland. In connection with this question, the author considered it necessary to refer to some medical-historical findings of earlier times.

Afferent Pathways↗
PubMed2004

Extrabulbar olfactory system and nervus terminalis FMRFamide immunoreactive components in Xenopus laevis ontogenesis.

The extrabulbar olfactory system (EBOS) is a collection of nerve fibers which originate from primary olfactory receptor-like neurons and penetrate into the brain bypassing the olfactory bulbs. Our description is based upon the application of two neuronal tracers (biocytin, carbocyanine DiI) in the olfactory sac, at the cut end of the olfactory nerve and in the telencephalon of the developing clawed frog. The extrabulbar olfactory system was observed already at stage 45, which is the first developmental stage compatible with our techniques; at this stage, the extrabulbar olfactory system fibers terminated diffusely in the preoptic area. A little later in development, i.e. at stage 50, the extrabulbar olfactory system was maximally developed, extending as far caudally as the rhombencephalon. In the metamorphosing specimens, the extrabulbar olfactory system appeared reduced in extension; caudally, the fiber terminals did not extend beyond the diencephalon. While a substantial overlapping of biocytin/FMRFamide immunoreactivity was observed along the olfactory pathways as well as in the telencephalon, FMRFamide immunoreactivity was never observed to be colocalized in the same cellular or fiber components visualized by tracer molecules. The question whether the extrabulbar olfactory system and the nervus terminalis (NT) are separate anatomical entities or represent an integrated system is discussed.

Animals↗
PubMed1999

Olfactory ensheathing cells promote neurite extension from embryonic olfactory receptor cells in vitro.

The role of ensheathing cells, a macroglial cell type with a unique presence in the olfactory system, in the outgrowth of olfactory receptor cell neurites was explored in vitro. Glial cell cultures harvested from both the olfactory bulb nerve layer and the hippocampus were established and immunocytochemically characterized. The expression of the p75 low-affinity nerve growth factor receptor by ensheathing cells was used to distinguish them from other macroglial subpopulations. Results indicated that ensheathing cell cultures were approximately 80% pure. Olfactory receptor cells were cocultured with ensheathing or hippocampal glial cells or were seeded on laminin or poly-L-lysine as controls. Olfactory receptor cells extended the longest primary neurites when cocultured with ensheathing cells. Neurite extension on hippocampal glia and laminin was less extensive than that observed on ensheathing cells but higher than that on poly-L-lysine. The neurite outgrowth-promoting effect of ensheathing cells was, at least in part, mediated by diffusible factors, because olfactory receptor cell neurite extension could also be facilitated when receptor cells were cultured in ensheathing cell-conditioned media. In contrast, cortical neurons extended neurites of equivalent lengths on ensheathing and hippocampal glia. The results suggest that ensheathing cells may release factors that support the continuous outgrowth of olfactory receptor cell axons and, therefore, the capacity of this pathway to recover from injury.

Animals↗
PubMed2002

Role of nerve growth factor in the olfactory system.

Olfactory neurons are unique in the mammalian nervous system because of their capacity to regenerate in adult animals. It has been shown that olfactory receptor cells located in the olfactory epithelium are replaced on a continuous basis and in response to injury throughout the life span of most species. NGF, which is one of the neurotrophic factors, is present in many areas of the central and peripheral nervous system. It has been shown that NGF in the olfactory bulb plays a role in the survival of cholinergic neurons in the horizontal limb of the diagonal band (HDB). Recent studies of NGF in the olfactory bulb suggest that it is involved in the development, maintenance, and regeneration of olfactory receptor cells. In this study, we review reports examining the relationship between NGF in the olfactory bulb and neuronal regeneration and development in the mammalian olfactory systems. Low- and high-affinity NGF receptor immunoreactivity is markedly expressed during regeneration and at different stages of development in the mouse olfactory system. This level of immunoreactivity is no longer present after completion of regeneration and at maturation. Other findings indicate that NGF injected into the olfactory bulb is transported retrogradely to the olfactory epithelium. It has also been shown that continuous anti-NGF antibody injection into the olfactory bulb causes degeneration and olfactory dysfunction. Administration of NGF directory into nasal cavity results in an increase in the expression of olfactory marker protein within the olfactory epithelium in axotomized rats. These findings suggested that the presence of NGF in the olfactory bulb plays an essential role in regeneration, maintenance, and development in the olfactory system of mammals.

Animals↗
PubMed1995

Mechanism of neuroinvasion of Venezuelan equine encephalitis virus in the mouse.

Venezuelan equine encephalitis virus (VEE) causes a biphasic disease in mice following subcutaneous inoculation in the footpad. In the initial phase, virus replicates primarily in the lymphoid tissues and induces a high titer viremia. Subsequently, the virus invades the central nervous system (CNS) from the circulation, and an encephalitis ensues. At the earliest times that VEE specific in situ hybridization signal was observed in the CNS, it was in areas of the brain involved in olfaction, leading to the hypothesis that virus may invade the brain from the circulation through the olfactory system. The results presented in this paper define the route of CNS invasion in experimental murine VEE disease initiated by subcutaneous inoculation. Virus circulating in the blood appears to seed specific areas of the peripheral nervous system during the viremic lymphoid phase of the illness. Virus replication within olfactory and dental tissues is followed by centripetal spread of virus along neural pathways. Virus enters the brain in a pattern reflecting the proximity of the peripheral invasion site to the CNS. Specifically, virus is first found in the brain within the structures of the olfactory system, followed by areas innervated by the trigeminal nerve. Virus later disseminates along fiber tracts and connected circuits within the brain, resulting in a disseminated meningoencephalitis. Surgical or chemical interruption of the olfactory system at the level of the olfactory neuroepithelium or the main olfactory bulb inhibited entry of VEE into the CNS through the olfactory nerve. However, the olfactory route is not absolutely required for CNS invasion, as virus invaded the CNS of olfactory ablated animals through the trigeminal nerve. These observations are consistent with a model of hematogenous seeding of the peripheral nervous system, followed by invasion of the CNS by direct neural spread.

Animals↗