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V M Carr

Publications and source records attributed to V M Carr.

6 recordsLinked to original sources
PubMed1992

Ablation of the olfactory bulb up-regulates the rate of neurogenesis and induces precocious cell death in olfactory epithelium.

Young adult rats were unilaterally bulbectomized and tritiated thymidine ([3H]TdR) was injected at variable times following surgery to determine the effect of bulbectomy on the rates of cell proliferation and cell death in the olfactory epithelium. Removal of the olfactory bulb elicits a two- to fourfold increase in the proliferation rate of ipsilateral olfactory epithelial cells 7-50 days following surgery. On the contralateral side, there was a temporary twofold increase in the proliferation rate during the second week after surgery, but this returned to control values at 3 weeks. This temporary increase was in parallel with the response on the ipsilateral side so that the ratio between operated and unoperated sides remained at two. Cell death in olfactory epithelium is also up-regulated following bulbectomy. Death of cells can occur as early as 1 day following incorporation of [3H]TdR, i.e., well before the sensory neurons become mature. This means there is an over-production of sensory cells, and they die at all stages of their life cycle. The number of cells dying is greater after bulbectomy, indicating that the overproduction of olfactory cells is more pronounced after surgery.

Animals↗
PubMed1991

Rat olfactory neurons express a 200 kDa neurofilament.

Neurofilament expression in peripheral olfactory neurons of adult rats was investigated by immunoblotting and immunohistochemistry using monoclonal antibodies specific for each of the 3 neurofilament proteins. Immunoblotting analysis of olfactory epithelium extracts demonstrated the presence of only the 200 kDa (NFH) polypeptide; the 68 kDa (NFL) and 160 kDa (NFM) neurofilaments were not detected. Similarly, no immunoreactivity was observed in tissue sections using the NFL and NFM antibodies. In contrast, when sections were probed with the antibody to NFH, immunoreactivity was localized primarily in the dendritic knobs and near the cell bodies of the receptor cells.

Animals↗
PubMed1991

Identification of a new non-neuronal cell type in rat olfactory epithelium.

We have examined adult and embryonic rat olfactory epithelia by immunohistochemical techniques using the monoclonal antibody 1A-6, which was raised against embryonic rat olfactory epithelia. A heretofore unidentified cell type, reactive with the monoclonal antibody 1A-6, was observed scattered within the epithelium. The 1A-6 reactivity of these cells is most intense on the microvilli projecting from the luminal cell surfaces. For several reasons, we believe these cells are not neurons but a distinct subpopulation of supporting cells or some other sort of non-neuronal cells. (1) They have no identifiable axonal process, are not reactive with an antibody against olfactory marker protein, and are not in juxtaposition with trigeminal axons. (2) They survive ablation of the olfactory bulb. (3) Their nuclei lie within the supporting cell layer, and they resemble supporting cells morphologically and in their [3H]thymidine birthdating and turnover characteristics. However, the 1A-6-positive cells fail to react with the general supporting cell-specific monoclonal antibody SUS-1 [see Hempstead J. L. and Morgan J. I. (1983) Brain Res. 188, 289-295] a finding which suggests that they are not typical supporting cells. Immunoreactivity to 1A-6 is developmentally regulated. Immunohistochemical preparations of almost all tissues we examined showed widespread reactivity in the embryo but a much more restricted pattern in the adult. In the olfactory epithelium of the fetus, the luminal surfaces of all cells, including supporting cells and olfactory receptor cells and cilia, are reactive, while in the adult only the non-neuronal cell subpopulation shows this reactivity. We also found that during the reconstitution of olfactory epithelium which occurs in response to olfactory bulbectomy-induced neuronal degeneration, fetal patterns of 1A-6 reactivity are not re-expressed, i.e. the only 1A-6-positive cells are the non-neuronal cells seen in unperturbed adult olfactory epithelium. Preliminary biochemical analyses of membrane fractions from E19 brain and from adult olfactory mucosa indicate that the 1A-6 reactivity is associated with two bands, having molecular weights of 42,000 and 46,000 on Western blots.

Age Factors↗
PubMed1978

Proliferative and degenerative events in the early development of chick dorsal root ganglia. I. Normal development.

Development of the chick dorsal root ganglia was examined in 4.5- to 9.5-day embryos. Tritiated thymidine (3H-TdR) and autoradiography was used to analyze proliferative activity and the Feulgen procedure to analyze degenerative activity in ganglia 12-17. Proliferative activity was found to be elevated through 4.5 days of incubation when as many as 14% of the ganglionic cells become labelled following a one-hour exposure to 3H-TdR. By 6.5 to 7.5 days proliferative activity decreases to 2-4% in the lateroventral (LV) regions and to approximately 1% in the mediodorsal (MD) regions of the ganglia. However, there appears to be increased proliferative activity by the end of the experimental period at 9.5 days. Birthdate studies demonstrate that large-scale neuronal production occurs between 4.5 and 6.5 days in the LV regions and between 4.5 and 7.5 days in the MD regions. After those times ganglionic proliferative activity must be largely nonneuronal in nature. This nonneuronal proliferation is greater in LV than in MD regions and in brachial than in nonbrachial ganglia. Degenerative activiy was found to be absent from the ganglia until after 4.5 days of incubation. It then increases rapidly, and by 5.5 days 5% of the LV cells in nonbrachial ganglia are degenerating. Degenerative activity then declines but is still present at 9.5 days. In contrast to results of an earlier study (Hamburger and Levi-Montalcini, '49), degenerative activity was also found in the LV region of brachial ganglia and the MD regions of brachial and nonbrachial ganglia. The pattern of LV degenerative activity in brachial ganglia is similar to that in nonbrachial ganglia, but the level of activity is lower. In the MD regions degenerative activity increases throughout the experimental period, and by 9.5 days as many as 4% of the MD cells are degenerating.

Age Factors↗
PubMed1978

Proliferative and degenerative events in the early development of chick dorsal root ganglia. II. Responses to altered peripheral fields.

Responses of chick embryo dorsal root ganglia to early wing bud amputation were examined histologically using tritiated thymidine (3H-TdR) and autoradiography to analyze proliferation and the Feulgen procedure to visualize degenerating cells. Right wing buds were amputated at stage 15 or 16. At 4.5 to 9.5 days of incubation embryos were given a 1-hour exposure to 3H-TdR and fixed. Feulgen-stained autoradiographs were examined for percentage of cells labelled (labelling index) or degenerating (degeneration index) in lateroventral (LV) and mediodorsal (MD) regions of brachial (G14-16) and nonbrachial (G12, 13, 17) ganglia. The earliest response to amputation was a highly significant increase in degeneration indices of LV and MD regions of ipsilateral brachial ganglia at 5.5 days. Significant brachial LV responses were observed throughout the remainder of the experimental period. Two peaks occur in this response: at 5.5 days, corresponding to the peak seen in normal nonbrachial ganglia, and at 8.5 days, having no counterpart in normal development. In brachial MD regions significant degenerative responses occur at most times examined. Significant responses also occur at 7.5 and 8.5 days in MD regions of nonbrachial ganglia. The presence of MD responses in our material indicates that maturation of at least some MD neurons occurs earlier than previously thought. Significant labelling responses occur in brachial LV regions from 7.5 days on. Because other studies (Carr and Simpson, '78a) show that this time is after the end of large-scale neuronal production, this labelling response must be nonneuronal in nature. We conclude that this response is a secondary response to amputation, consequent to the greatly increased cellular degeneration. Results of experiments involving addition of limb buds at the brachial level are also presented.

Amputation, Surgical↗