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PubMed1985

Olfactory marker protein in the human olfactory pathway.

The presence of olfactory marker protein (OMP) in the olfactory tissue of rats, gerbils, and humans was demonstrated with goat antiserum to rat OMP. In control studies on rat neural tissue, OMP was found to be located in the olfactory receptor cells, nerves, and bulbs. Likewise, staining of OMP was found in the olfactory tissues of gerbils. Olfactory marker protein reactivity was also demonstrated in human olfactory receptor cells, nerves, and bulbs. The reactivity of OMP in human olfactory neurons to goat antiserum has allowed determination of the exact junction of olfactory and respiratory epithelia immunohistochemically.

Aged↗
PubMed1985

Injured neurons in the olfactory bulb of the adult rat grow axons along grafts of peripheral nerve.

Certain neurons in the central nervous system (CNS) of adult mammals extend axons for several cm along peripheral nerve grafts inserted into the brain or spinal cord. It is not clear, however, if these nerve cells constitute a special population or are examples of a general capacity of the injured mammalian CNS to regrow processes under these experimental conditions. Furthermore, because the new axons could originate by collateral sprouting from uninjured neurons, it is important to prove that the interruption of a central axonal projection can be followed by extensive fiber regrowth from the damaged neurons. In this anatomical study, we examined whether: (1) nerve cell type; and (2) axotomy, influence CNS axon regrowth along peripheral nerve grafts. For this purpose, we grafted segments of sciatic nerve into the olfactory bulb (OB) of adult rats and used combinations of neuroanatomical tracers (horseradish peroxidase and the fluorescent dyes True Blue and Nuclear Yellow) to investigate axonal regrowth from the different neurons that normally populate the OB. We demonstrate that OB axons extending along peripheral nerve grafts originate from mitral and tufted cells near the graft tip, rather than from the smaller OB neurons (periglomerular, short axon, and granule cells). Most of the mitral and tufted cells that extend new axons in grafted peripheral nerve segments lose their normal projections through the lateral olfactory tract because of axotomy at the time of grafting. Neuronal type, damage, and proximity to the graft appear to be prerequisites of this regenerative response from the OB.

Animals↗
PubMed1993

Glial progenitor cells of the nerve fiber layer of the olfactory bulb: effect of astrocyte growth media.

There are two morphologically distinct types of glial cells (i.e., ensheathing cells and astrocytes) in the nerve fiber layer (NFL) of the adult mammalian olfactory bulb. Ensheathing cells provide ensheathment for olfactory axons, whereas astrocytes occupy the interfascicular spaces of the olfactory NFL. During embryonic development, however, only one type of glial cell is found in this layer of the olfactory bulb, namely, the ensheathing cell. Even though ensheathing cells take up residence within the CNS, they are actually derived from the olfactory placode. Far less is known about the developmental origin of interfascicular astrocytes, which arise either from the glial progenitor cells that give rise to ensheathing cells or from astrocyte precursor cells that migrate into the NFL from deeper layers of the bulb primordium. In the present study, enriched populations of ensheathing cells were grown in vitro in media known to promote the growth and differentiation of astrocytes to determine whether ensheathing cell progenitors could differentiate into astrocytes. These media failed to induce the appearance of astrocytes in the ensheathing cell cultures. It was concluded that the astrocytes of the NFL most likely arise from progenitor cells that migrate into this layer from deeper parts of the developing bulb.

Animals↗
PubMed1992

Immunocytochemical demonstration of neural cell adhesion molecule (NCAM) along the migration route of luteinizing hormone-releasing hormone (LHRH) neurons in mice.

Contact between the developing forebrain and the ingrowing central processes of the olfactory, vomeronasal and terminal nerves is preceded by a migration of neural cell adhesion molecule (NCAM)-immunoreactive cells from the epithelium of the olfactory pit and the formation of an NCAM-immunoreactive cellular aggregate in the mesenchyme between the olfactory pit and the forebrain. The axons of the olfactory, vomeronasal, and terminal nerves, also NCAM-immunoreactive, grow into the cellular aggregate, which as development proceeds, becomes continuous with the rostral tip of the forebrain. The lateral and more rostral part of the cellular aggregate receives the ingrowing axons of the olfactory nerves and becomes the olfactory nerve layer of the olfactory bulb. The medial, more caudal part receives the central processes of the vomeronasal and terminal nerves. The vomeronasal nerve ends in the accessory olfactory bulb. The central processes of the terminal nerve end in the medial forebrain. Luteinizing hormone-releasing hormone (LHRH)-immunoreactive neurons, like the vomeronasal and terminal nerves, originate from the medial part of the olfactory pit. These LHRH cells migrate into the brain along and within a scaffolding formed by the NCAM-immunoreactive axons of the vomeronasal and terminal nerves, and they are never seen independent of this NCAM scaffold as they cross the nasal lamina propria. The results suggest that: (1) NCAM is likely to be necessary for scaffold formation, and (2) the scaffold may be essential for the subsequent migration of LHRH neurons into the brain. Because they aggregate, migrating LHRH-immunoreactive neurons, on which we did not detect NCAM immunoreactivity, may interact via other cell adhesion molecules (CAM). Inasmuch as the interaction between the LHRH-immunoreactive neurons and the NCAM-immunoreactive scaffold is heterotypic, the possibility of a heterophilic (NCAM to other CAM) interaction is not ruled out. These findings focus our attention on the functional role of NCAM in this migratory system.

Animals↗
PubMed1994

Olfactory mucosa of patients with olfactory disturbance following head trauma.

The olfactory mucosa in 7 patients with olfactory disturbance following head trauma were sampled for biopsy with special biopsy forceps and examined by immunohistochemical staining with anti-neuron-specific enolase (NSE) and S-100 protein (S-100) antibodies. The residual olfactory receptor cells and nerve bundles were counted, and the degree of degeneration was determined. In 5 patients, olfactory receptor cells that reacted with anti-NSE antiserum remained, although the number varied with the patient, and in 2 patients the receptor cells disappeared. In the lamina propria, the S-100-immunoreactive olfactory nerves were retained in 6 patients. The outcome was poor in all cases regardless of the number of residual receptor cells and nerve bundles. These results indicate that the degree of impairment of the peripheral olfactory region after head trauma differs from case to case, and that even if the receptor cells and nerve bundles remain, it is difficult to improve the condition, although some cases of malingering may be contained.

Adolescent↗