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S L Youngentob

Publications and source records attributed to S L Youngentob.

At least 19 recordsLinked to original sources
PubMed2003

Mucosal activity patterns as a basis for olfactory discrimination: comparing behavior and optical recordings.

In over half a century numerous studies have demonstrated that different odorants produce individually different spatial patterns of neural receptor activity on the olfactory mucosa. However, the thought that these differential activity patterns could be the neural code underlying olfactory perception has not been tested directly. In the present study using operant techniques, rats were trained to differentially identify five odors from a homologous series of iso-intensive straight-chain aldehydes that differed serially by only one carbon atom, viz. hexaldehyde to decaldehyde. The rats identified each of the five odorants with greater than 90% correct identification. The degree of perceptual similarity between any pair of the five odorants was determined. Using multidimensional scaling techniques (MDS) the similarity measures yielded a two-dimensional perceptual odorant space. Optical techniques were used to record the olfactory mucosal activity patterns in response to these same five iso-intensive aldehydes. The mucosal activity elicited by each odorant revealed individually distinct band-like patterns that varied both within and across these bands. More importantly, the relative differential responsivity of the bands was related to chain length. An MDS analysis of the dissimilarity measure between all possible pairs of odorant induced activity patterns yielded a two-dimensional neurophysiologic odorant space. Further analysis indicated that the neurophysiologic and psychophysically determined odorant spaces were highly correlated (F(1,39)=23.9, P=nil). These results give additional credence to the concept that the odorant-induced mucosal activity patterns may serve as the substrate for the perception of odorant quality.

Aldehydes↗
PubMed2003

OMP gene deletion results in an alteration in odorant-induced mucosal activity patterns.

Previous behavioral work, using a complex five-odorant identification task, demonstrated that olfactory marker protein (OMP) is critically involved in odor processing to the extent that its loss results in an alteration in odorant quality perception. Exactly how the lack of OMP exerts its influence on the perception of odorant quality is unknown. However, there is considerable neurophysiological evidence that different odorants produce different spatiotemporal patterns of neural activity at the level of the mucosa and that these patterns predict the psychophysically determined perceptual relationship among odorants. In this respect, OMP gene deletion is known to result in a constellation of physiologic defects (i.e., marked reduction in the electroolfactogram (EOG) and altered response and recovery kinetics) that would be expected to alter the odorant-induced spatiotemporal activity patterns that are characteristic of different odorants. This, in turn, would be expected to alter the spatiotemporal patterning of information that results from the mucosal projection onto the bulb, thereby changing odorant quality perception. To test the hypothesis that odorant-induced mucosal activity patterns are altered in mice lacking the gene for OMP, we optically recorded the fluorescent changes in response to odorant stimulation from both the septum and turbinates of both OMP-null and control mice using a voltage-sensitive dye (di-4-ANEPPS Molecular Probes, Eugene, OR) and a Dalsa 120 x 120, 12-bit CCD camera. To maintain continuity with the previous behavioral work, the odorants 2-propanol, citral, carvone, ethylacetoacetate, and propyl acetate were again used. Each odorant was randomly presented to each mucosal surface in a Latin-Square design. The results of this study demonstrated that, for both mouse strains, there do indeed exist different spatiotemporal activity patterns for different odorants. More importantly, however, these patterns significantly differed between OMP-null and control mice. That is, although the general regions of characteristic activity for different odorants were the same in both mouse strains, the patterns in the null animals were degraded relative to controls. These data suggest therefore that the alterations in mucosal activity may serve as the substrate for the behaviorally observed changes in odorant quality perception in the null mutant.

Animals↗
PubMed2001

OMP gene deletion results in an alteration in odorant quality perception.

To test the hypothesis that odorant quality perception is altered in olfactory marker protein (OMP)-null mice, we trained and tested adult OMP-null and control mice, using a 5-odorant identification confusion matrix task (animal odorant confusion matrix [AOCM]). On average, control and null mice performed the task at equivalent levels. The composite 5 x 5 response matrix from 40 testing sessions for each subject (both OMP-null and control) was compared with that of every other subject, yielding a dissimilarity matrix of AOCM responses. A multidimensional scaling (MDS) analysis of the dissimilarity data yielded a 4-dimensional solution, with each mouse occupying a point in MDS animal space. Statistical analysis demonstrated significant effects of genotype in determining the location of a mouse in the MDS space. These data suggest, therefore, that compared with that of controls, odorant quality perception is altered in the OMP-null mouse.

Animals↗
PubMed2001

Intranasal inoculation with the olfactory bulb line variant of mouse hepatitis virus causes extensive destruction of the olfactory bulb and accelerated turnover of neurons in the olfactory epithelium of mice.

Viral upper respiratory infections are the most common cause of clinical olfactory dysfunction, but the pathogenesis of dysosmia after viral infection is poorly understood. Biopsies of the olfactory mucosa in patients that complain of dysosmia after viral infection fall into two categories: one in which no olfactory epithelium is seen and another in which the epithelium is disordered and populated mainly by immature neurons. We have used intranasal inoculation with an olfactory bulb line variant of MHV to study the consequences of viral infection on peripheral olfactory structures. MHV OBLV has little direct effect on the olfactory epithelium, but causes extensive spongiotic degeneration and destruction of mitral cells and interneurons in the olfactory bulb such that the axonal projection from the bulb via the lateral olfactory tract is markedly reduced. Moreover, surviving mitral cells apparently remain disconnected from the sensory neuron input to the glomerular layer, judging from retrograde labeling studies using Dil. The damage to the bulb indirectly causes a persistent, long-term increase in the turnover of sensory neurons in the epithelium, i.e. the relative proportion of immature to mature sensory neurons and the rate of basal cell proliferation both increase. The changes that develop after inoculation with MHV OBLV closely resemble the disordering of the olfactory epithelium in some patient biopsies. Thus, damage to the olfactory nerve or bulb may contribute to a form of post-viral olfactory dysfunction and MHV OBLV is a useful model for studying the pathogenesis of this form of dysosmia.

Administration, Intranasal↗
PubMed2001

Functional consequences following infection of the olfactory system by intranasal infusion of the olfactory bulb line variant (OBLV) of mouse hepatitis strain JHM.

The present study assessed the functional consequences of viral infection with a neurotropic coronavirus, designated MHV OBLV, that specifically targets central olfactory structures. Using standard operant techniques and a 'go, no-go' successive discrimination paradigm, six BALB/c mice were trained to discriminate between the presentation of an air or odor stimulus (three mice for each of the odorants propanol and propyl acetate). Two additional BALB/c mice were trained to discriminate between the presentation of air and the presentation of either vanillin or propionic acid. Following criterion performance, each mouse received an additional 2000 trials of overtraining. At completion of overtraining one mouse from the propanol and propyl acetate groups were allocated as untreated. The remaining six mice were inoculated with 300 microl of the OBLV stock per nostril for a total of 1.5 x 10(6) p.f.u. in 600 microl. Following a 1 month rest, untreated and inoculated animals were again tested on their respective air versus odor discrimination task. Untreated animals immediately performed at criterion levels. In contrast, inoculated animals varied in their capacity to discriminate between air and odorant. Five of the six inoculated mice showed massive disruption of the olfactory bulb, including death of mitral cells; the other was more modestly affected. In addition, the density of innervation of the olfactory mucosa by substance P-containing trigeminal fibers is also affected by inoculation. Those mice that remained anosmic to the training odorants had the most severe reduction in mitral cell number and substance P fiber density among the inoculated animals.

Administration, Intranasal↗
PubMed1999

Reinnervation of the rat olfactory bulb after methyl bromide-induced lesion: timing and extent of reinnervation.

We used the inhalation of methyl bromide gas to produce a near-complete destruction of the rat olfactory epithelium and analyzed the reinnervation of the bulb during reconstitution of the epithelium. The degeneration of olfactory axons elicits a transient up-regulation of glial cell proliferation and glial fibrillary acidic protein expression in the olfactory nerve and olfactory nerve layer of the bulb. Anterograde transport after intranasal infusion of wheat germ agglutinin conjugated horseradish peroxidase demonstrates that the first nascent axons reach the bulb within the first week after lesion. Subsequently, a massive wave of fibers arrives at the bulb between 1 and 2 weeks postlesion, and enters the glomeruli between 2 and 3 weeks postlesion. However, the olfactory projection does not stabilize until 8 weeks after lesion judging from the return in growth associated protein-43 expression to control levels. The extent of reinnervation after lesion is correlated with the completeness with which the epithelium reconstitutes itself. In rats that are lesioned while fed ad libitum, there is near-complete reconstitution of the neuronal population, and the projection onto the bulb fills the glomerular layer in its entirety. However, in rats that are lesioned while food restricted, a significant fraction of olfactory epithelium becomes respiratory during its reconstitution, and the population of reinnervating fibers is less. As a consequence, the posterior half of the bulb remains hypoinnervated overall and denervated at its caudal margin. The preferential reinnervation of the anterior bulb in the food-restricted, methyl bromide gas-lesioned animals indicates that the mechanisms that guide the growth of the olfactory axons and restore receptotopy do not operate with the same precision in this setting as they do during development or during the lower level of turnover associated with the "normal" laboratory existence. Accordingly, we hypothesize that the persistence of a significant population of pre-existing neurons is needed to preserve receptotopy during reinnervation. In addition, the results suggest that in the face of massive turnover and a reduced afferent population, there is a tendency for reinnervating axons to fill available synaptic space.

Animals↗
PubMed1999

OMP gene deletion causes an elevation in behavioral threshold sensitivity.

To characterize the behavioral consequences of OMP gene deletion on odor processing we assessed the ability of OMP-null animals to acquire an air vs odor discrimination for five odorants, and determined whether OMP-null animals differed from controls in their threshold sensitivity to the odorant propanol. On average, control and OMP-null animals did not differ in the number of testing sessions needed to achieve criterion performance on each discrimination problem (2.04 vs 1.68, respectively; t=0.83, p=0.41). However, null animals were significantly less sensitive to the odorant propanol (3.01 x 10(-8) vs 1.06 x 10(-5), respectively; t=4.09, p=0.015). These in vivo behavioral results provide support for the hypothesis that OMP plays a modulatory role in the odor detection/signal transduction process.

Animals↗
PubMed1998

Adult olfactory epithelium contains multipotent progenitors that give rise to neurons and non-neural cells.

We have infused replication-incompetent retroviral vectors into the nasal cavity of adult rats 1 day after exposure to the olfactotoxic gas methyl bromide (MeBr) to assess the lineage relationships of cells in the regenerating olfactory epithelium. The vast majority of the retrovirus-labeled clones fall into three broad categories: clones that invariably contain globose basal cells (GBCs) and/or neurons, clones that always include cells in the ducts of Bowman's glands, and clones that are composed of sustentacular cells only. Many of the GBC-related clones contain sustentacular cells and horizontal basal cells as well. Most of the duct-related clones contain gland cells, and some also include sustentacular cells. Thus, the destruction of both neurons and non-neuronal cells that is caused by MeBr activates two distinct types of multipotent cells. The multipotent progenitor that gives rise to neurons and non-neuronal cells is a basal cell, whereas the progenitor that gives rise to duct, gland, and sustentacular cells resides within the ducts, based on the pattern of sparing after lesion and the analysis of early regeneration by using cell type-specific markers. We conclude that the balance between multipotency and selective neuropotency, which is characteristic of globose basal cells in the normal olfactory epithelium, is determined by which cell types have been depleted and need to be replenished rapidly.

Animals↗
PubMed1998

Transplantation of multipotent progenitors from the adult olfactory epithelium.

Mammalian olfactory epithelium produces new neurons rapidly throughout adulthood. Here, we demonstrate that precursor cells harvested from the adult olfactory epithelium, when transplanted into the nasal mucosa of host rats exposed previously to an olfactotoxic gas, engraft and participate in neuroepithelial reconstitution. In contrast to their normal neuronal fate in situ, grafted precursors harvested from bulbectomized donors produced non-neuronal cells as well as neurons. These results demonstrate that epithelial precursors activated following olfactory bulbectomy are not irreversibly committed to making neurons. Thus, olfactory progenitors are subject to a form of feedback control in vivo that regulates the types of cells that they produce within a broader-than-neuronal repertoire.

Alkaline Phosphatase↗
PubMed1997

Odorant threshold following methyl bromide-induced lesions of the olfactory epithelium.

The present study assessed the functional consequences of peripheral olfactory destruction on the minimum detectable levels of stimulation for the odorants 2-propanol, D-limonene, and ethyl acetoacetate. Using standard operant techniques, eight Long-Evans rats were trained to criterion on an air versus odor differential response task. Odorant threshold was then determined on 10 consecutive testing sessions, using a computer-automated olfactometer and psychophysical tracking procedure. Following the last testing session, the rats were lesioned by exposing them to 330 ppm methyl bromide gas for 6 h. For each lesioned animal the anatomical state of the olfactory epithelium was evaluated relative to behavioral performance on the odorant threshold task at 3 days postlesion. For the group of rats, a comparison of pre- and postlesion performance demonstrated that, on the average, odor sensitivity was not altered by lesions that destroy roughly 95-98% of the epithelium. However, analysis of individual cases illustrated that two of the eight rats showed an elevation in odor sensitivity, albeit minimally, that was considered different from the prelesion performance. For those animals affected, we could extract no apparent relationship between the behavioral findings and the extent of anatomical damage. The results of this study demonstrate the remarkable capacity of the olfactory system to maintain normal or near-normal detection sensitivity in the face of massive damage. This capacity presumably reflects both the normal exposure of the epithelium to continual injury and the importance of maintained olfactory function for the survival of the animal.

1-Propanol↗
PubMed1996

The aging olfactory epithelium: neurogenesis, response to damage, and odorant-induced activity.

Olfactory epithelium retains the capacity to recover anatomically after damage well into adult life and perhaps throughout its duration. None the less, olfactory dysfunctions have been reported widely for elderly humans. The present study investigates the effects of aging on the neurophysiological and anatomical status of the olfactory epithelium in barrier-raised Fischer 344X Brown Norway F1 hybrid rats at 7, 10, 25 and 32/35 months old. The posterior part of the olfactory epithelium in 32/35-month-old rats is well preserved. Globose basal cells are dividing, and new neurons are being born even at this advanced age. None the less, the numbers of proliferating basal cells and immature, GAP-43 (+) neurons are significantly decreased. Neurophysiological status was evaluated using voltage-sensitive dye techniques to assess inherent patterns of odorant-induced activity in the epithelium lining the septum and the medial surface of the turbinates. In middle and posterior zones of the epithelium, there were neither age-related changes in overall responsivity of this part of the olfactory epithelium to any of five odorants, nor shifts in the location of the odorant-induced hotspots. The inherent activity patterns elicited by the different odorants do become more distinct as a function of age, which probably reflects the decline in immature neurons and a slight, but not statistically significant, increase in mature neurons as a function of age. In contrast with the excellent preservation of posterior epithelium, the epithelium lining the anterodorsal septum and the corresponding face of the turbinates is damaged in the 32/35-month-old animals: in this part, horizontal basal cells are reactive, more basal cells and sustentacular cells are proliferating than in younger animals or in posterior epithelium of the same animals, and the neuronal population is less mature on average. Our findings indicate that degeneration of the olfactory epithelium is not an inevitable or pre-programmed consequence of the aging process, since the posterior zone of the epithelium is very well preserved in these barrier-protected animals. However, the deterioration in the anterior epithelium suggests that environmental insults can accumulate or become more severe with age and overwhelm the regenerative capacity of the epithelium. Alternatively, the regenerative capacity of the epithelium may wane somewhat with age. Either of these mechanisms or some combination of them can account for the functional and anatomical deterioration of the sense of smell associated with senescence in humans.

Action Potentials↗
PubMed1995

Reconstitution of the rat olfactory epithelium after methyl bromide-induced lesion.

The olfactory epithelium and its neuronal population are known to have a substantial capacity to recover after either direct injury or damage to the olfactory nerve. However, the mechanisms underlying that capacity for recovery, and indeed the limits on the recovery process, are not well understood. The aim of this study is to describe in detail the way in which the olfactory epithelium reconstitutes after direct injury. Adult male rats were exposed to 330 ppm methyl bromide (MeBr) gas for a single 6-hour period. The exposure destroys all of the neurons and sustentacular cells in over 95% of the olfactory epithelium of food-restricted rats and in over 90% of the epithelium in ad-libitum-fed rats of the same weight, yet substantial recovery of the olfactory epithelium occurs. In response to the lesion, cellular proliferation increases markedly beginning between 24 and 48 hours, peaks at 1 week, and persists at levels higher than the control level for more than 4 weeks after MeBr exposure. Even though proliferation accelerates promptly, the beginning of neuronal reconstitution is delayed; only a few immature neurons are observed 3 days after the lesion, yet they reappear in large numbers by the end of the first week. The first mature neurons emerge between 7 and 14 days after lesion and increase to near normal numbers by 4-6 weeks. In association with the restoration of the neuronal population, basal cell proliferation returns to control levels between 4 and 6 weeks after damage. Likewise, sustentacular cells, identifiable by anticytokeratin 18 labeling, reappear rapidly and reform a distinct lamina in the superficial aspect of the epithelium. They closely resemble their counterparts in control epithelium with regard to disposition and shape by 3 weeks after lesion and with regard to expression of olfactory-specific cytochrome P450s by 8 weeks. Thus, most areas of the epithelium are restored to a near normal appearance and cellular composition by the end of 8 weeks, suggesting that the MeBr paradigm for lesioning the epithelium offers significant advantages over techniques such as Triton X-100 or ZnSO4 irrigation. However, not all measures of epithelial status are normal even at 8 weeks. Immature neurons remain slightly more numerous than normal at this time. Furthermore, some areas of the olfactory epithelium do not recover after MeBr lesion and are replaced by respiratory epithelium.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1995

Enhancement of odorant-induced mucosal activity patterns in rats trained on an odorant identification task.

Previous studies have demonstrated that there are intrinsic spatial patterns of odorant sensitivity across the rat olfactory mucosa. The question of how these patterns are determined and whether they are modifiable with experience remains open. Therefore, the present study examined whether the odorant-induced spatial activity patterns which are characteristic of different odorants would be altered by experience. Odorant exposure was achieved as a consequence of training and testing on a five odorant identification task in which rats were trained to differentially report (i.e. identify) the odorants propanol, ehtylacetoacetate, carvone, citral, and propyl acetate. At the completion of testing, each animal was sacrificed and their mucosal activity patterns recorded using optical techniques and a voltage-sensitive dye. Using the dye, di-4-ANEPPS, we monitored the fluorescence changes at 100 contiguous sites with a 10 x 10 photodiode array on the olfactory mucosa of each rat's septum and medial surface of the turbinates in response to the same five odorants. The recorded spatial activity patterns of trained animals were compared to those of age-matched controls. For the trained animals, both mucosal surfaces showed a significant increase in the average response magnitude. Furthermore, for the septal mucosa only, there was a significant increase in the distinctiveness of an odorant's characteristic 'hot spot'.

1-Propanol↗
PubMed1995

Mucosal inherent activity patterns in the rat: evidence from voltage-sensitive dyes.

1. Fluorescence changes in the dye di-4-ANEPPS were monitored on the rat's nasal septum and medial surface of the turbinates in response to odorant stimuli. For each mucosal surface a 6.0 x 6.0-mm area was sampled at 100 contiguous sites with a 10 x 10 photodiode array. The odorants were propyl acetate, 2-propanol, citral, L-carvone and ethylacetoacetate, each presented at a low and high concentration. 2. Like previous work using optical recording techniques and potential-sensitive dyes on the amphibian epithelium, the fluorescence signals elicited by odorant stimuli in the rat preparation were nearly identical in shape, time course, and response characteristics as the electroolfactogram (EOG). As with the EOG, a response could only be recorded in the presence of odorant stimuli (that is, no response was detected when nonodorized, humidified air was presented as the stimulus); the amplitude depended on odorant concentration, and the response was abolished both by ether and Triton X-100. 3. Although the entire expanse of each sampled tissue (i.e., septum and medial surface of the turbinates) responded to stimulation with each odorant, each stimulus induced a distinct spatial pattern of activity that was independent of odorant concentration and consistent from animal to animal. Furthermore, the spatial activity patterns recorded for the septum were mirror images of those recorded from the medial surface of the turbinates. 4. Formal statistical analysis of the loci of maximal activity or "hot spot" indicated highly significant effects of the odorants for both the septum and medial surface of the turbinates. 5. The results of these studies give further support to the hypothesis that odorant quality is encoded by differential spatial activity patterns in the olfactory epithelium that are characteristic of different odorants.

Animals↗
PubMed1995

Odorant-specific spatial patterns in mucosal activity predict perceptual differences among odorants.

1. Using operant techniques, rats were trained to differentially report (i.e., identify) the odorants propanol, carvone, citral, propyl acetate, and ethylacetoacetate. After acquisition training, the animals were tested using a 5 x 5 confusion matrix design. The results of the behavioral tests were used to measure the degree of perceptual dissimilarity between any pair of odorants. These dissimilarity measures were then subjected to multidimensional scaling analysis to establish a two-dimensional perceptual odor space for each rat. 2. At the completion of behavioral testing, the fluorescence changes in the dye di-4-ANEPPS were monitored on the rat's nasal septum and medial surface of the turbinates in response to the same odorants. For each mucosal surface a 6.0 x 6.0 mm area was sampled at 100 contiguous sites with a 10 x 10 photodiode array. 3. Formal statistical analysis indicated a highly significant predictive relationship between the relative position of an odorant's mucosal loci of maximal activity or "hot spot" and the relative position of the same odorant in a psychophysically determined perceptual odor space (F = 15.6, P < 0.001). 4. The results of this study suggest for the first time that odorant-induced mucosal activity patterns serve as the substrate for the perception of odorant quality.

Animals↗
PubMed1994

On the formation of neuromata in the primary olfactory projection.

Olfactory axons have been shown to grow aberrantly and form dense collections of axons, termed neuromas, in the olfactory epithelium of rats in which the olfactory bulb was ablated. Likewise, in human olfactory mucosa, collections of neurites have been noted in a variety of disease states, including Alzheimer's disease. We report here an immunohistochemical and electron microscopic analysis of aberrant axonal growth in the rat olfactory mucosa induced by experimental lesion. In particular, we have used the monoclonal antibody 2G12, which binds to the phosphorylated form of GAP-43, as an extremely sensitive marker for neuromatous axons, because it does not label neuronal cell bodies. In unilaterally bulbectomized rats, neuromas form in posterior olfactory epithelium on the operated side. Several lines of evidence, including serial section reconstruction, indicate that olfactory axons are induced to grow back into the epithelium at a distance from their point of origin as a consequence of bulbectomy, and are accompanied by glial cells from the olfactory nerve. Avulsion of a part of the olfactory nerve has similar effects as destruction of the olfactory bulb. Intraepithelial neuromas also develop in the olfactory mucosa of rats simultaneously exposed to methyl bromide gas and injected with 3-methyl indole; this treatment severely damages the olfactory epithelium directly. Exposure to methyl bromide alone causes milder damage, and the neuromas that form are transient. The evidence indicates that neuromas form after the epithelium is directly damaged because axons are trapped in the epithelium. Both of the mechanisms identified here should be taken into account when considering the findings in the human olfactory mucosa.

Animals↗
PubMed1994

Retroviral lineage studies of the rat olfactory epithelium.

Replication-incompetent retroviral vectors that encode the heritable marker enzyme, beta-galactosidase, were used to study the lineage relationships of cells in the olfactory epithelium of unmanipulated animals and in the olfactory epithelium as it reconstitutes after lesion. Virally-marked cells are categorized as to type based on their position in the epithelium and on expression of NCAM (limited to neurons) and the carbohydrate moiety recognized by Griffonia lectin (limited to the dark/horizontal basal cells and the microvillar class of supporting cells). Direct injections of the vectors into the olfactory epithelium of otherwise intact animals produce clusters of beta-galactosidase-labeled cells when assessed 6-10 days after infection; these clusters are composed of neurons and NCAM-negative/lectin-negative light/globose basal cells exclusively. In contrast, clusters of virally-marked cells after MeBr-induced lesion of the epithelium frequently contain both neurons and supporting cells, as well as both types of basal cells. Other clusters contain supporting cells and/or Bowman's gland/duct cells. It is likely that the clusters of marked cells are derived from a single founder cell, i.e. the cells are clonal and lineally related, since the clusters are widely dispersed. Furthermore, infusion of mixtures of viruses that can be distinguished on the basis of the type and subcellular localization of the marker enzyme that is expressed produce clusters that are homogenous with respect to enzyme type, providing strong evidence in favor of the notion that the clusters are clonal in nature. Thus, the founders of the clones that contain neurons, supporting cells and basal cells are pluripotent in their capacity for differentiation. It is unlikely that the pluripotent cells are found in Bowman's gland/duct, since we have yet to observe a clone that contains neurons and cells in Bowman's gland/duct. Hence, the pluripotent stem cells are to be found in the basal cell compartment of the epithelium. However, the exact nature of these stem cells remains unknown and a subject for future investigation.

Animals↗