There are at least two basal cell populations in the olfactory epithelium that could give rise to olfactory neurons during development, in the normal adult, and after experimentally induced receptor cell death. These populations have been subdivided as horizontal (HBC) and globose (GBC) basal cells on the basis of morphological criteria and by staining with antibodies against cytokeratin. HBCs are positive for cytokeratin while GBCs are negative. We have studied which cell type is induced to divide during receptor cell regeneration stimulated by olfactory bulbectomy using a combination of immunocytochemistry and autoradiography. By examining which population increases its labeling index with 3H-thymidine (3H- TdR) at various times after bulbectomy, it is shown that there is an increase in 3H-TdR uptake in the cytokeratin-negative GBCs with no change in the cytokeratin-positive HBCs. This suggests that the GBCs are specifically induced to divide in response to cues that accompany receptor cell death, and it is thus concluded that these cells are among the precursors of new olfactory receptor neurons.
We thank Mr. Walter Dent for photography and Ms. Barbara D'Angelo for preparation of the manuscript. We thank Dr. Charles A. Greer for many helpful and stimulating discussions and for reading of the manuscriot.
In the salamander olfactory bulb, mitral output cells exhibit a variety of responses to electrical and odor stimulation, but the cellular interactions within the bulb that give rise to these responses are not completely understood. We have developed a computer model to investigate whether available data are sufficient for formulating a simulated bulb circuit that can generate realistic mitral cell output. A set of coupled difference equations incorporating mathematical descriptions of anatomical and physiological data was used to calculate changes in membrane potentials of olfactory bulb neurons over time. Model mitral cells showed responses to simple orthodromic and antidromic electrical stimuli that were similar to salamander intracellular responses. Without changing the parameters of the equations, simulated odor stimuli were applied that elicited complex patterns of mitral depolarization, spike activation, and hyperpolarization that emerged from the interactions among the numerous elements in the model. As with the electrical stimuli, model mitral responses to odor were also strikingly similar to those of real mitral cells. As an initial test of how different circuit components contribute to the responses, the lateral interactions between mitral cells and bulbar interneurons were manipulated. Tests with reduced lateral interactions and other tests with no inhibitory synaptic connections both produced mitral cell outputs that were uncharacteristic of salamander recordings. The similarity of the model's output to the complex properties of salamander single-cell recordings suggests that several critical features of the bulb circuit responsible for shaping mitral cell responsivity have been captured.(ABSTRACT TRUNCATED AT 250 WORDS)
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