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PubMed1994

Evidence for glutamate as the olfactory receptor cell neurotransmitter.

1. Synaptic transmission between olfactory receptor neurons and mitral/tufted cells was examined using a whole-cell recording technique in a hemisected preparation of the turtle olfactory bulb. To determine the olfactory receptor neuron transmitter, we isolated components of the synaptic response of mitral/tufted cells to olfactory nerve stimulation using postsynaptic receptor antagonists. 2. Low-intensity stimulation of the olfactory nerve evoked monosynaptic excitatory postsynaptic potentials in mitral/tufted cells that consisted of a rapid and prolonged depolarization with little contribution from other bulb neurons. The exogenous application of glutamate mimicked the response of mitral/tufted cells to olfactory nerve stimulation. 3. Olfactory nerve stimulation evoked in mitral/tufted cells a two component response that was reversibly blocked by glutamate receptor antagonists. The first, a rapid depolarization of short duration, was sensitive to the non-N-methyl-D-aspartate (NMDA) receptor antagonist 6,7-dinitroquinoxaline-2,3-dione (DNQX); the second, a depolarization of slower onset but longer duration, was sensitive to the NMDA receptor antagonist DL-2-amino-5-phosphonovaleric acid (AP5). When DNQX and AP5 were both present the postsynaptic response was completely abolished. These results strongly support the notion that glutamate is the neurotransmitter at the olfactory nerve to mitral/tufted cell synapse.

Animals↗
PubMed2006

Immunocytochemical localization of the GABAB2 receptor subunit in the glomeruli of the mouse main olfactory bulb.

The olfactory input to the brain is carried out by olfactory nerve axons that terminate in the olfactory bulb glomeruli and make synapses onto dendrites of glutamatergic projection neurons, mitral and tufted cells, and GABAergic interneurons, periglomerular cells. The dendrites are reciprocally connected through asymmetric synapses of mitral/tufted cells with periglomerular cells and symmetric synapses of the opposite direction. Transmission at the first synapse in the olfactory pathway is regulated presynaptically, and this regulation is mediated, in part, by metabotropic GABAB receptors that, when activated, inhibit transmitter release from the olfactory nerve. Functional GABAB receptors are heterodimers composed of the GABAB1 and GABAB2 subunits. Studies using double immunofluorescence have shown colocalization of both subunits in the glomerular neuropil, and ultrastructural studies have localized GABAB1 to extrasynaptic, synaptic, and perisynaptic sites on the plasma membrane of olfactory nerve terminals. We studied the subcellular localization of GABAB2 in the mouse olfactory glomeruli using a subunit-specific antibody and preembedding immunogold labeling. Immunoreactivity for GABAB2 was associated with symmetric dendrodendritic synapses of periglomerular cells with mitral/tufted cells and was localized to the extrasynaptic plasma membrane of presynaptic dendrites, and extrasynaptic, synaptic, and perisynaptic sites on the plasma membrane of postsynaptic dendrites. The results suggest that postsynaptic, and perhaps presynaptic, GABAB receptors may be expressed at GABAergic synapses between dendrites of periglomerular interneurons and projection neurons. Immunolabeling was observed at junctions of the olfactory nerve with mitral/tufted cell dendrites, providing ultrastructural evidence for the expression of the GABAB2 subunit at the primary olfactory synapse.

Animals↗
PubMed1976

Degenerative and regenerative processes in the olfactory system of homing pigeons.

Experimental resection of the olfactory nerve in the homing pigeon induces a total degeneration of the nerve and olfactory epithelium. The orthograde degenerative process starts before the retrograde one. Ten days after resection, new neurons begin to differentiate from the basal cells. The axon forms earlier than the distal dendritic process, and the speed of growth increases slowly. The regenerated axons only reach the bulb in the 5th month. Two months after resection the olfactory epithelium is similar to that of the intact control side. The ultrastructural features of the mucosa and olfactory axons are similar to those of normal ones.

Animals↗
PubMed1982

Impulse activity in presynaptic dendrites: analysis of mitral cells in the isolated turtle olfactory bulb.

Impulse activity has been reported in neuronal dendrites in several regions of the central nervous system, where it is believed to assist in boosting transmission of signals from remote dendritic sites to the cell body. We have studied this activity in the dendrites of mitral cells in an isolated preparation of the turtle olfactory bulb. Intracellular recordings have been obtained from mitral cells responding to single volleys in the olfactory nerves or lateral olfactory tract. In addition to the large somatic spike, a small fast prepotential (FPP) was present in nearly all cells in response to an orthodromic volley in the olfactory nerves, but it was never seen in antidromic responses from the lateral olfactory tract. Collision tests using antidromic and orthodromic volleys showed that the EPP does not propagate into the axon. Hyperpolarizing current injections caused delay and blocking of the soma spike with little effect on the FPP response. These and other tests provided evidence to localize the EPP in the dendrites and to distinguish it from injury potentials and from spikes in the axon hillock or axonal initial segment. These results suggest that one function of the impulse in mitral cell dendrites is the classical one of boosting transmission of synaptic responses from the glomerular tuft to the cell body. In addition, it si well established that mitral cell dendrites are presynaptic to the dendrites of interneurons within the bulb and that these connections provide pathways for recurrent inhibition of the mitral cells. It therefore appears that the dendritic impulse in mitral cells acts as a booster for local dendritic synaptic output. These results provide further evidence for the multiple state-dependent input-output functions of cells with presynaptic dendrites.

Action Potentials↗
PubMed1994

Ontogenetic development of gonadotropin-releasing hormone-like immunoreactive neurons in the brain of the chum salmon, Oncorhynchus keta.

In the chum salmon, gonadotropin-releasing hormone-immunoreactive (GnRH-ir) cells were first detected in the olfactory placode of embryos at 16 days after fertilization, and then appeared sequentially in the olfactory nerve and the distal part of the forebrain by hatching. Four months after hatching, the terminal nerve was differentiated along the olfactory nerve, and GnRH-ir fibers extended to the hypothalamus and hypophysis. GnRH-ir cells occurred later in the preoptic area in about 1-year-old juveniles. These data suggest that GnRH neurons originate in the olfactory placode and then migrate into the brain along the olfactory nerve.

Aging↗
PubMed1996

Migration of GnRH-immunoreactive neurons from the olfactory placode to the brain: a study using avian embryonic chimeras.

Previous studies suggest that gonadotropin-releasing hormone (GnRH) neurons appear in the olfactory placode and subsequently migrate into the brain during embryonic development. The aim of the present study was to obtain direct evidence for migration of GnRH neurons from the olfactory placode into the brain. Olfactory placodes from quail embryos were transplanted isotopically and isochronically, to replace the unilaterally ablated olfactory placodes of chick embryos. The chimeric embryos were allowed to develop for several days until they reached the embryonic stages when GnRH neurons are seen in the brain in normal embryos. Quail olfactory epithelia were formed in the host chick embryos. Quail olfactory nerves were also formed and reached the olfactory bulb or primordial olfactory bulb. GnRH-immunoreactive cells of quail origin revealed by a triple staining method were observed in the quail olfactory epithelium, quail olfactory nerve, chick olfactory bulb, and septo-preoptic area. These results indicate that GnRH neurons originate in the olfactory placode and migrate into the telencephalon including the septo-preoptic area. A migratory route of GnRH neurons was well documented by the use of a quail neuron-specific antibody, QN. The migratory route in the brain is discussed with special reference to the terminal nerve. A GnRH-immunoreactive neuronal group of chick origin appeared in the diencephalon of chimeric embryos. These diencephalic neurons may be of non-placodal origin. FMRFamide-immunoreactive neurons of quail origin were also found in the quail olfactory nerve and the host olfactory bulb, suggesting that FMRFamide neurons also originate in the olfactory placode and migrate into the brain.

Animals↗
PubMed1996

Expression of extracellular matrix molecules in the embryonic rat olfactory pathway.

Primary olfactory neurons arise from placodal neuroepithelium that is separate from the neuroepithelial plate that forms the neural tube and crest. The axons of these neurons course along a stereotypical pathway and invade the rostral telencephalic vesicle where they induce the formation of the olfactory bulb. In the present study we examined the expression of several extracellular matrix constituents during formation of the olfactory nerve pathway in order to identify putative developmentally significant molecules. Double-label immunofluorescence was used to simultaneously map the trajectory of growing primary olfactory axons by expression of growth associated protein 43 (GAP-43) and the distribution of either laminin, heparan sulfate proteoglycans (HSPG), or chondroitin sulfate proteoglycans (CSPG). At embryonic day 12.5 (E12.5) primary olfactory axons have exited the olfactory neuroepithelium of the nasal pit and formed a rudimentary olfactory nerve. These axons together with migrating neural cells form a large mass outside the rostral surface of the telencephalon. This nerve pathway is clearly defined by a punctate distribution of laminin and HSPG. CSPG is selectively present in the mesenchyme between the olfactory nerve pathway and the nasal pit and in the marginal zone of the telencephalon. At E14.5 primary olfactory axons pierce the telencephalon through gaps that have emerged in the basement membrane. At this age both laminin and HSPG are colocalized with the primary olfactory axons that have entered the marginal zone of the telencephalon. CSPG expression becomes downregulated in this same region while it remains highly expressed in the marginal zone adjacent to the presumptive olfactory bulb. By E16.5 most of the basement membrane separating the olfactory nerve from the telencephalon has degraded, and there is direct continuity between the olfactory nerve pathway and the central nervous system. This strict spatiotemporal regulation of extracellular matrix constituents in the olfactory nerve pathway supports an important role of these molecules in axon guidance. We propose that laminin and HSPG are expressed by migrating olfactory Schwann cells in the developing olfactory nerve pathway and that these molecules provide a conducive substrate for axon growth between the olfactory neuroepithelium and the brain. CSPG in the surrounding mesenchyme may act to restrict axon growth to within this pathway. The regional degradation of the basement membrane of the telencephalon and the downregulation of CSPG within the marginal zone probably facilitates the passage of primary olfactory axons into the brain to form the presumptive nerve fiber layer of the olfactory bulb.

Animals↗
PubMed1998

Transport and subcellular distribution of nickel in the olfactory system of pikes and rats.

Occupational exposure to nickel by inhalation may result in impaired olfactory sense. Recent studies have shown that nickel is transported from the olfactory epithelium along the axons of the primary olfactory neurons to the brain. In the present study 63Ni2+ was applied in the olfactory chambers of pikes (Esox lucius) and the rate at which the metal was transported in the primary olfactory neurons was determined by beta-spectrometry. The results showed a wave of 63Ni2+ in the olfactory nerves, which slowly moved toward the olfactory bulbs. The maximal 63Ni2+ transport rate corresponding to the movement of the base of the wave front was found to be about 0.13 mm/h at the experimental temperature (10 degrees C). This rate of 63Ni2+ transport falls into the class of slow axonal transport. Radioluminography of tape sections of a pike given 63Ni2+ in the right olfactory chamber showed a selective labeling of the right olfactory nerve. The subcellular distribution of 63Ni2+ in the olfactory nerves and the olfactory epithelium of the pikes was studied in tissues subjected to homogenizations and centrifugations, and these methods were also used to examine the subcellular distribution of 63Ni2+ in tissues of the olfactory system of rats given the metal intranasally. It was found that the 63Ni2+, in both the pike and the rat, was present in the cytosol and also in association with various particulate cell constituents. Gel filtrations of the cytosols showed that the 63Ni2+ mainly was eluted at a Ve/Vo ratio corresponding to a MW of about 250. The same coefficient was obtained in gel filtrations performed with 63Ni2+ mixed with histidine in vitro. It is likely that the cytosolic nickel may be bound to histidine or possibly to other amino acids which are similar in size to histidine. Additionally, in the olfactory tissues of the rat the 63Ni2+ was partly present in the cytosol in association with a component with a MW of about 25,000. It is concluded that (i) 63Ni2+ is transported in the primary olfactory neurons by means of slow axonal transport, (ii) in this process the metal is bound to both particulate and soluble cytosolic constituents, and (iii) the metal shows this subcellular distribution also in other parts of the olfactory system.

Animals↗
PubMed1996

High-speed optical imaging of afferent flow through rat olfactory bulb slices: voltage-sensitive dye signals reveal periglomerular cell activity.

Fast, multiple-site optical recording and video imaging techniques were combined to visualize the olfactory processing stream as it flowed through rat olfactory bulb slices stained with the voltage-sensitive dye RH155. A 464 element photodiode detector array was used to record the voltage-sensitive dye signals. Focal electrical stimulation of the olfactory nerve layer evoked relatively large optical responses in the olfactory nerve and glomerular layers but only small responses within the external plexiform layer. With paired-pulse stimulation, glomerular attenuation was evident in signals recorded from the glomerular and external plexiform layers but not from the olfactory nerve layer. At very high recording speeds ( < 0.2 msec/frame), the presynaptic component of the olfactory processing stream could be followed as it flowed through the olfactory nerve layer and into the glomerular layer, where its amplitude rapidly declined. This decline was followed by a reciprocal rise in a postsynaptic depolarization that was largely restricted to the glomerular layer. Spatiotemporal interactions between overlapping afferent streams within the glomerular layer were observed and partially characterized. The optically recorded glomerular layer response was largely resistant to bath application of GABAA receptor antagonists but was sensitive to manipulations of external chloride concentration and to bath application of a stilbene derivative, 4-acetamido-4'isothiocyanatostilbene-2,2'-disulfonic acid known to block Cl- conductances. It is suggested the the voltage-sensitive dye signals recorded from the glomerular layer reflect activity in periglomerular cells and that Cl- efflux through non-GABAA chloride channels contributes to the postsynaptic depolarization of these cells after olfactory nerve stimulation.

Afferent Pathways↗
PubMed1986

Functional properties of vertebrate olfactory receptor neurons.

The interaction of an odorant with the chemosensitive membrane of olfactory receptor neurons initiates a sequence of molecular and membrane events leading to sensory transduction, impulse initiation, and the transmission of sensory information to the brain. The main steps in this sequence are summarized in Figure 6. Several lines of evidence support the hypothesis that the initial molecular events and subsequent stages of transduction are mediated by odorant receptor sites and associated ion channels located in the membrane of the cilia and apical dendritic knob of the olfactory receptor neuron. Similarly, the membrane events associated with impulse initiation and propagation are mediated by voltage-gated channels located in the initial axonal segment and the axolemma. The ionic and electrical events associated with the proposed sequence have been characterized in general using a variety of experimental techniques. The identification, localization, and sequence of membrane events are consistent with the neurophysiological properties observed in specific regions of the bipolar receptor neuron. The influence of other cells in the primary olfactory pathway such as the sustentacular cells in the olfactory epithelium, the Schwann cells in the olfactory nerve, and the astrocytes in the olfactory nerve layer in the olfactory bulb on the physiological activity of the olfactory receptor neuron is an emerging area of research interests. The general principles derived from the experimental results described in this review provide only a framework that is both incomplete and of necessity somewhat speculative. As noted in the Introduction, the multidisciplinary study of the primary olfactory pathway is undergoing a renaissance of research interest. The application of modern biophysical, cell, and molecular biological techniques to the basic issues of odorant recognition and membrane excitability will clarify the speculations and lead to the establishment of new hypotheses. Three broad areas of research will benefit from such studies. First, the application of biophysical techniques will lead to a detailed characterization of the membrane properties and associated ion conductance mechanisms. Second, the isolation and biochemical characterization of intrinsic membrane and cytosolic proteins associated with odorant recognition, sensory transduction, and the subsequent electrical events will result from the utilization of cell and molecular biological techniques.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗
PubMed1996

Transplanted glial scar impedes olfactory bulb reinnervation.

The olfactory system is the only region of the mammalian central nervous system in which degeneration of the primary sensory neurons results in the development of new neurons and reinnervation of the secondary sensory neurons. Axotomy of the olfactory nerve at the cribriform plate does not cause the formation of a glial scar which blocks nerve regeneration. The purpose of this study was to determine whether a glial scar that formed in the optic nerve would suppress axonal regeneration when transplanted to the site of olfactory nerve axotomy. Primary olfactory neurons were axotomized along the cribriform plate in adult rats. A compact glial scar formed by transection of an adult rat optic nerve 50 to 60 days prior to removal was transplanted into the olfactory nerve axotomy site. The rats were allowed to survive for 1, 2, 3, or 4 weeks. Transport of horseradish peroxidase (HRP) from the nasal cavity by the olfactory neurons was used to examine the temporal and spatial pattern of regeneration of the olfactory nerve after axotomy and axotomy followed by glial scar transplantation. Twenty-one days after olfactory nerve axotomy, HRP was found in the glomerular layer where the primary olfactory axons synapse on the apical dendrites of the secondary olfactory neurons. In the presence of the transplanted glial scar, HRP labeling was not found in certain glomeruli even at 4 weeks postaxotomy. Glial scars formed within the optic nerve impede reinnervation of the olfactory bulb by neurons which have an exceptional regenerative capacity due in part to the ensheathing glia.

Age Factors↗
PubMed2000

Focal denervation alters cellular phenotypes and survival in the developing rat olfactory bulb.

Several studies have demonstrated that contact between the olfactory nerve and the forebrain is critical for normal olfactory bulb development. Removal of the embryonic olfactory placode results in a failure of the olfactory bulb to form, as well as causing other forebrain malformations. The current study introduces a technique that permits removal of contact between specific regions of the olfactory nerve and the bulb early in development, without causing damage to other brain regions, and without removing the peripheral olfactory organ. The manipulation, which involves insertion of a small Teflon chip between the cribriform plate and the bulb, prohibits growth of new axons into the "shadow" region behind the implant. Focal denervation of the olfactory bulb causes a decrease in bulb and layer sizes, a reduction in mitral cell number, and changes to bulb architecture. Using a battery of antibodies (OMP, MAP2, TuJ1, calretinin, calbindin, parvalbumin, TH, and GAD), we further demonstrated that 1) focal denervation alters the relationship between the olfactory nerve and the bulb, 2) the fine structure of cells in denervated regions is disrupted, and 3) cellular phenotypes change in response to loss of afferent contact. These results suggest that contact between the olfactory nerve and the bulb is important for maintaining bulb architecture and cell survival, structure, and phenotype. They also point to focal denervation as a useful technique for examining the role of neural contact in olfactory development and maintenance of the central nervous system.

Animals↗
PubMed2001

Olfaction preservation in anterior cranial base approaches: an anatomic study.

OBJECTIVE: To study the anatomic basis for olfaction-sparing anterior cranial base approaches. METHODS: The medial anterior skull base containing the olfactory unit and delimited by the inner table of the frontal sinus, the lesser wing of the sphenoid bone, and the medial orbital walls was removed from six cadaveric specimens. Histological methods were used to investigate the location, distribution, and depth of penetration of olfactory nerves. Hematoxylin and eosin and Gomori trichrome staining were used to visualize landmarks and architecture. S-100 neurofilament protein immunostaining was used to identify nerve fascicles and axons. In three cadaveric head specimens, olfaction-sparing craniofacial approaches were performed and the excised olfactory units were evaluated histologically. RESULTS: Bundles of olfactory nerves were identified primarily in the nasal septum; relatively fewer bundles could be identified in the middle turbinate. Olfactory nerve endings were identified up to 20 mm below the cribriform plate (range, 7-20 mm). The superior and middle nasal meatus were most innervated; olfactory innervation was virtually absent in the inferior nasal meatus. Histological evaluation of the olfactory unit elevated during olfaction-sparing techniques routinely revealed transection of olfactory nerves that exited the skull base. CONCLUSION: In olfaction-sparing anterior cranial base approaches, the olfactory nerves are inevitably transected. The clinical significance of olfactory nerve transection for postoperative functional recovery of olfaction remains to be analyzed.

Cadaver↗
PubMed2000

Chromogranin A-immunoreactive cells in the olfactory system of anuran amphibians.

Chromogranin A (CgA) is a member of the granin family of acidic proteins that are present in the secretory granules of many endocrine and neuroendocrine cells. The specific function(s) of these proteins is not known, but they seem to be the precursors of biologically active peptides, and they may act as helper proteins in the sorting and packaging of peptide hormones and neuropeptides. Using indirect immunohistochemistry, we have found CgA immunoreactivity in the primary olfactory epithelia, the vomeronasal epithelia, the olfactory nerves, and the olfactory bulbs of tadpoles of the American toad, Bufo americanus, and the green frog, Rana clamitans. CgA immunoreactivity was present in the early stages of larval development in toads but was not detected in toad tadpoles after the hindlimb buds formed or in toadlets or adults. In green frog tadpoles, CgA-immunoreactive cells were found in pre- and prometamorphic stages but not in late climax. CgA immunoreactivity was also absent in froglets, but it was detected in the vomeronasal epithelium but not the olfactory epithelium of adult green frogs.

Animals↗
PubMed1989

Development of the nerve fiber layer in the olfactory bulb of mouse embryos.

The purpose of this study was to provide an ultrastructural description of the development of the olfactory nerve fiber layer (ONL) in the olfactory bulbs of mouse embryos. The developmental age of each embryo was determined by means of the Theiler staging system. During stages 17 and 18, the olfactory axons grew through the mesenchyme toward the cerebral vesicle; they were accompanied by a group of electron-dense cells which were referred to as peripheral glial progenitor cells (GPCs) because they ensheathed the adjacent axons. In Theiler stage 19-21 embryos, the axons and the peripheral GPCs grew dorsocaudally along the external surface of the bulb primordium forming a presumptive ONL immediately superficial to its glia limitans. Through small breaks in this glia limitans, the axons, but not the peripheral GPCs, penetrated into the marginal zone of the bulb primordium. Even though by the first half of stage 21 there were only short stretches of glia limitans separating the presumptive ONL from the marginal zone, there was no intermingling of the perikarya between the two layers. A definitive ONL could be identified by the second half of Theiler stage 21, by which time the glia limitans of the bulb primordium had totally disappeared. However, up to Theiler stage 24 of development the only cells to be found in this definitive ONL were the peripheral GPCs. Although in Theiler stage 25 and 26 embryos there was an additional population of less-electron-dense GPCs within the definitive ONL, these cells were likely derived from the previous group of peripheral GPCs rather than from cells newly emigrated from the deeper layers of the developing bulb. This developmental data necessitated a reevaluation of the cell lineages of the two glial cell types that reside within the ONL of the adult olfactory bulb.

Aging↗
PubMed1986

Neurons of the olfactory epithelium in adult rats contain vimentin.

In the developing nervous system, the intermediate filament protein vimentin is found in the proliferating neuroepithelium and neural crest. As development proceeds, postmitotic neurons cease vimentin expression and neurofilament proteins begin to accumulate. We have shown that olfactory receptor neurons deviate from the general pattern of neuronal intermediate filament expression, in that they continue to express vimentin or a highly vimentin-like protein rather than neurofilament proteins in the adult rat. With light-microscopic immunohistochemistry, three independently derived antibodies to vimentin label all portions of the primary olfactory projection, including the sensory neuron cell bodies in the olfactory epithelium, the fascicles of the olfactory nerve, and their axonal arbors in the glomeruli of the olfactory bulb. In contrast, anti-neurofilament antisera stain only rare scattered receptor cells and a small number of axons in the olfactory nerve. Electron-microscopic immunohistochemistry shows dense staining of olfactory axons with anti-vimentin. The vimentin-like immunoreactive material in the olfactory nerve layer was characterized by SDS-PAGE and by immunoblotting. On immunoblots of homogenates of the olfactory nerve, the anti-vimentin monoclonal antibody SBV-21 (Blose et al., 1984) stains only a single protein of Mr = 55 kDa. This band comigrates with vimentin in crude cytoskeletal material from the neonatal rat brain prepared according to the method of Dahl et al. (1981). SBV-21 does not stain neurofilament triplet proteins or glial fibrillary acidic protein, which are also present in these blots. These results demonstrate that the vast majority of olfactory receptor neurons and their axons contain vimentin or a protein of similar immunological character and electrophoretic mobility, while identifiable expression of neurofilament proteins is confined to a very small subpopulation. Hence, the switch in intermediate filament proteins that normally accompanies neuronal maturation is arrested in most olfactory neurons, and a "juvenile" biochemical marker is retained. This population of neurons is also unique among mammalian neurons in several other respects, including that olfactory neurons die during normal adult life or following injury and then are replaced from a proliferating pool of stem cells.

Age Factors↗
PubMed1992

Expression of the dopaminergic phenotype in the olfactory bulb: neither calcitonin gene-related peptide nor olfactory input is necessary.

In the olfactory bulb, expression of tyrosine hydroxylase (TH) in juxtaglomerular neurons is dependent on innervation by the olfactory nerve. The presence of the neuropeptide calcitonin gene-related peptide (CGRP) within the olfactory nerve has led to the hypothesis that CGRP is responsible for regulation of TH expression in the bulbar neurons. On the other hand, other investigators claim that olfactory receptors never produce CGRP and that functional contact with olfactory axons regulates production of TH by bulbar neurons. Two different experimental procedures were used to test whether either CGRP or contact with the olfactory nerve is essential for production of TH by bulbar neurons in vivo. The peptidergic innervation of the olfactory bulb was eliminated either by neonatal capsaicin treatment, or by stereotaxic, electrolytic lesions of the ophthalmic division of the trigeminal nerve. Both of the treatments leave the olfactory innervation of the bulb intact while eliminating the CGRP-immunoreactive fibers in the olfactory nerve and glomeruli. Subsequent immunocytochemistry reveals a normal complement of bulbar TH-immunoreactive juxtaglomerular neurons in the absence of peptidergic innervation. In order to test whether olfactory nerve input is necessary for expression of TH in vivo, the anlage of the olfactory bulb was removed from embryonic (E16) rat pups and transplanted into the anterior chamber. These ectopic olfactory bulbs, although devoid of olfactory nerve input, contain numerous TH-immunoreactive neurons. Thus olfactory nerve input is not necessary for expression of TH in bulbar neurons.

Afferent Pathways↗
PubMed1994

Removal of olfactory placode prevents the development of LHRH neurons in the forebrain of the chick embryo: possible interaction between migrating LHRH neurons and highly polysialylated form of neural cell adhesion molecule (NCAM-H).

A unilateral olfactory placodectomy prevented the development of LHRH- and NCAM-H-expressing neurons as well as NCAM-H expressing olfactory nerve on the operated side, whereas the development of LHRH- and NCAM-H-expressing neurons and olfactory nerve was not disturbed. In the embryos with an incomplete olfactory placodectomy, a small number of LHRH-immunoreactive (ir) cells expressing NCAM-H were detected in the olfactory epithelial fragments and in the NCAM-H-positive olfactory nerve remants which ceased to extend their axons to the forebrain. The lack of the central projection of the olfactory nerve caused stagnation of LHRH-ir cells, no LHRH-ir cells being found in the forebrain. These results clearly suggest the importance of the structural support for the migration of LHRH-ir cells. Furthermore, the migrating LHRH-ir cells deviated from the poorly developed olfactory nerve and migrated not only to the central direction but also to the peripheral direction of the NCAM-H-positive medial nasal branch of the ophthalmic nerve of the trigeminal nerve. This suggests that the migration route of the LHRH neurons is not programmed in detail in the precursor cells of LHRH neurons in the olfactory placode. Since the migrating LHRH-ir cells were never independent of NCAM-H-positive neural elements in the operated embryos, it is suggested that not only the structural support for the migration but also the possible interaction between the migration of LHRH-ir cells and NCAM-H and/or other unknown factors may be needed for successful LHRH neuronal migration.

Animals↗