The ultrastructure of the saccus vasculosus of teleost fishes III supporting tissue, innervation, vascularization

1971 ◽  
Vol 19 (4) ◽  
pp. 327 ◽  
Author(s):  
WJR Lanzing ◽  
Lennep EW van

The ultrastructure of the supporting cells, the nerve fibres, and the blood vessels of the saccus vasculosus was investigated. Apart from the apical protuberance, the coronet cells are usually enveloped by thin sheets of supporting-cell cytoplasm. Although pinocytotic vesicles were not evident, the distal region of the supporting cells often contains cytoplasmic vesicles. The possibility of transfer of fluid by these cells is discussed. The network of nerve fibres contains both vesiculated and non-vesiculated nerve endings. Some of these endings lie adjacent to coronet cells and, occasionally, to supporting cells. In considering the function of the coronet cell undue emphasis was probably placed in the past on the possible possession of an axon and, also, on the vicarious presence of a secretory product in the lumen of the saccus vasculosus. It is suggested that the coronet cell could function as a chemoreceptor monitoring the composition of the cerebrospinal fluid.

1981 ◽  
Vol 89 (4) ◽  
pp. 638-645 ◽  
Author(s):  
Scott A. Estrem ◽  
Richard W. Babin ◽  
Jai H. Ryu ◽  
Kenneth C. Moore

Cochleas from 12 guinea pigs were evaluated using light, scanning, and transmission electron microscopy after systemic administration of cis-diamminedichloroplatinum (cis-DDP). Administration of cis-DDP resulted in loss of the Preyer reflex and degeneration of outer hair cells (OHC) with increased dose. The OHC degeneration was most pronounced in the basal turns of the cochlea with greatest severity in the inner row. Ultrastructural evidence of OHC degeneration included dilatation of the parietal membranes, softening of the cuticular plate, increased vacuolization and increased numbers of lysosome-like bodies in the apical portion of the cell. Supporting cells appeared more sensitive than OHC. Alteration of supporting cell ultrastructure preceded detectable change in OHC. Injury to the supporting cells was noted with intracellular vesiculation and increased autophagocytosis.


2019 ◽  
Author(s):  
Jingyuan Zhang ◽  
Daxiang Na ◽  
Miriam Dilts ◽  
Kenneth S. Henry ◽  
Patricia M. White

AbstractNoise induced hearing loss (NIHL) affects over ten million adults in the United States, and there is no biological treatment to restore endogenous function after damage. We hypothesized that activation of signaling from ERBB2 receptors in cochlear supporting cells could mitigate NIHL damage. We used the Tet-On genetic expression system to drive a constitutively active variant of ERBB2 (CA-ERBB2) in cochlear supporting cells three days after permanent noise damage in young adult mice. Hearing thresholds were assessed with auditory brainstem response tests prior to noise damage, and hearing recovery was assessed over a three month period. We evaluated supporting cell proliferation, inner and outer hair cell (IHC and OHC) survival, synaptic preservation, and IHC cytoskeletal alterations with histological techniques. Mice harboring CA-ERBB2 capability had similar hearing thresholds to control littermates prior to and immediately after noise exposure, and incurred similar levels of permanent hearing loss. Two and three months after noise exposure, CA-ERBB2+ mice demonstrated a partial but significant reversal of NIHL threshold shifts at the lowest frequency tested, out of five frequencies (n=19 total mice, p=0.0015, ANOVA). We also observed improved IHC and OHC survival (n=7 total cochleae, p=5 × 10−5, Kruskal-Wallis rank sum test). There was no evidence for sustained supporting cell proliferation. Some mortality was associated with doxycycline and furosemide treatments to induce the Tet-ON system. These data suggest that ERBB2 signaling in supporting cells promotes HC repair and some functional recovery. Funded by NIH R01 DC014261, and grants from the Schmitt Foundation and UR Ventures.


1967 ◽  
Vol 2 (3) ◽  
pp. 349-358
Author(s):  
R. M. EAKIN ◽  
JANE A. WESTFALL ◽  
M. J. DENNIS

The eye of a nudibranch, Hermissenda crassicornis, was studied by light and electron microscopy. Three kinds of cells were observed: large sensory cells, each bearing at one end an array of microvilli (rhabdomere) and at the other end an axon which leaves the eye by the optic nerve; large pigmented supporting cells; and small epithelial cells, mostly corneal. There are five sensory cells, and the same number of nerve fibres in the optic nerve. The receptor cells contain an abundance of small vesicles, 600-800 Å in diameter. The lens is a spheroidal mass of osmiophilic, finely granular material. A basal lamina and a capsule of connective tissue enclose the eye. In some animals the eye is ‘infected’ with very small bodies, 4-5 µ in diameter, thought to be symbionts.


2019 ◽  
Vol 10 (1) ◽  
Author(s):  
Barbara Nicol ◽  
Sara A. Grimm ◽  
Frédéric Chalmel ◽  
Estelle Lecluze ◽  
Maëlle Pannetier ◽  
...  

Abstract Sex determination of the gonads begins with fate specification of gonadal supporting cells into either ovarian pre-granulosa cells or testicular Sertoli cells. This fate specification hinges on a balance of transcriptional control. Here we report that expression of the transcription factor RUNX1 is enriched in the fetal ovary in rainbow trout, turtle, mouse, goat, and human. In the mouse, RUNX1 marks the supporting cell lineage and becomes pre-granulosa cell-specific as the gonads differentiate. RUNX1 plays complementary/redundant roles with FOXL2 to maintain fetal granulosa cell identity and combined loss of RUNX1 and FOXL2 results in masculinization of fetal ovaries. At the chromatin level, RUNX1 occupancy overlaps partially with FOXL2 occupancy in the fetal ovary, suggesting that RUNX1 and FOXL2 target common sets of genes. These findings identify RUNX1, with an ovary-biased expression pattern conserved across species, as a regulator in securing the identity of ovarian-supporting cells and the ovary.


2020 ◽  
Vol 117 (36) ◽  
pp. 22225-22236
Author(s):  
Xiao-Jun Li ◽  
Angelika Doetzlhofer

Mechano-sensory hair cells within the inner ear cochlea are essential for the detection of sound. In mammals, cochlear hair cells are only produced during development and their loss, due to disease or trauma, is a leading cause of deafness. In the immature cochlea, prior to the onset of hearing, hair cell loss stimulates neighboring supporting cells to act as hair cell progenitors and produce new hair cells. However, for reasons unknown, such regenerative capacity (plasticity) is lost once supporting cells undergo maturation. Here, we demonstrate that the RNA binding protein LIN28B plays an important role in the production of hair cells by supporting cells and provide evidence that the developmental drop in supporting cell plasticity in the mammalian cochlea is, at least in part, a product of declining LIN28B-mammalian target of rapamycin (mTOR) activity. Employing murine cochlear organoid and explant cultures to model mitotic and nonmitotic mechanisms of hair cell generation, we show that loss of LIN28B function, due to its conditional deletion, or due to overexpression of the antagonistic miRNAlet-7g, suppressed Akt-mTOR complex 1 (mTORC1) activity and renders young, immature supporting cells incapable of generating hair cells. Conversely, we found that LIN28B overexpression increased Akt-mTORC1 activity and allowed supporting cells that were undergoing maturation to de-differentiate into progenitor-like cells and to produce hair cells via mitotic and nonmitotic mechanisms. Finally, using the mTORC1 inhibitor rapamycin, we demonstrate that LIN28B promotes supporting cell plasticity in an mTORC1-dependent manner.


Cells ◽  
2019 ◽  
Vol 8 (10) ◽  
pp. 1266 ◽  
Author(s):  
Eszter Berekméri ◽  
Ádám Fekete ◽  
László Köles ◽  
Tibor Zelles

Exploring the development of the hearing organ helps in the understanding of hearing and hearing impairments and it promotes the development of the regenerative approaches-based therapeutic efforts. The role of supporting cells in the development of the organ of Corti is much less elucidated than that of the cochlear sensory receptor cells. The use of our recently published method of single-cell electroporation loading of a fluorescent Ca2+ probe in the mouse hemicochlea preparation provided an appropriate means to investigate the Deiters’ cells at the subcellular level in two different cochlear turns (apical, middle). Deiters’ cell’s soma and process elongated, and the process became slimmer by maturation without tonotopic preference. The tonotopically heterogeneous spontaneous Ca2+ activity less frequently occurred by maturation and implied subcellular difference. The exogenous ATP- and UTP-evoked Ca2+ responses were maturation-dependent and showed P2Y receptor dominance in the apical turn. By monitoring the basic structural dimensions of this supporting cell type as well as its spontaneous and evoked purinergic Ca2+ signaling in the hemicochlea preparation in different stages in the critical postnatal P5-25 developmental period for the first time, we showed that the soma and the phalangeal process of the Deiters’ cells go through age- and tonotopy-dependent changes in the morphometric parameters and purinergic signaling.


2018 ◽  
Vol 11 (1) ◽  
pp. 7-18
Author(s):  
Héctor Barrera Villa Zevallos ◽  
Robert Markham ◽  
Frank Manconi

Endometriosis is a gynaecological disease that occurs in approximately 10% to 15% of women of reproductive age and up to 47% of infertile women. The presence of implants of endometrial-like glands and stroma outside the uterus, characteristic of this disease, induce a wide variety of symptoms, mainly pelvic pain and infertility. Women suffering from this condition experience great distress, which significantly affects their quality of life. Numerous studies attempting to decipher the pathogenic mechanisms of endometriosis have been conducted around the world, yet its aetiology still remains unknown. It is widely believed that in women with endometriosis, the endometrium has characteristic features that allow the formation of implants once fragments have entered the peritoneal cavity through retrograde menstruation. Furthermore, a strong genetic tendency to develop the disease has been reported among patients and first-degree relatives. Thanks to the recent technological advances achieved in genomics and bioinformatics, a number of studies have had the potential to analyse several aspects of the pathogenesis of endometriosis from a genetic perspective. Due to the recent identification of nerve fibres in the endometrium of women with endometriosis, research on the neurogenesis of the disease has increased in the past few years. However, the genetic aspects of nerve growth in endometriosis have not been analysed in depth and further research providing important insights into the mechanisms that mediate pain in affected patients has the potential to contribute substantially to the future management of the condition.


1974 ◽  
Vol 83 (2) ◽  
pp. 192-201 ◽  
Author(s):  
Daniel H. Matulionis

Olfactory epithelium from three groups of C57B1/6J and SWR/J mice exposed once or twice daily to 10% cigarette smoke for six or nine days was examined at the ultrastructural level. Olfactory epithelium of SWR/J experimental mice was not affected by cigarette smoke. However, prominent alterations were noted in this epithelium of C57B1/6J smoke treated mice. These alterations included a reduction in size and (possibly) number of olfactory vesicles which sometimes failed to protrude above the epithelial surface and greatly reduced numbers of olfactory vesicle sensory cilia. In the supporting cell population an abnormal electron-lucent cell type was noted among the usually darker types. Both cell types were frequently found protruding abnormally above the epithelial surface. Microvilli of supporting cells were markedly reduced in number. The present study revealed that the olfactory epithelia in all mice of the same strain are not affected equally by acute smoke exposures. In affected animals the degree of morphological alteration suggests that normal olfaction might have been impaired. Strain differences in reaction to smoke insult indicate that susceptibility is genetically determined.


2018 ◽  
Author(s):  
Lu M. Yang ◽  
Kathryn S.E. Cheah ◽  
Sung-Ho Huh ◽  
David M. Ornitz

AbstractThe mouse organ of Corti develops in two steps: progenitor specification and differentiation. Fibroblast Growth Factor (FGF) signaling is important in this developmental pathway, as deletion of FGF receptor 1 (Fgfr1) or its ligand, Fgf20, leads to the loss of hair cells and supporting cells from the organ of Corti. However, whether FGF20-FGFR1 signaling is required during specification or differentiation, and how it interacts with the transcription factor Sox2, also important for hair cell and supporting cell development, has been a topic of debate. Here, we show that while FGF20-FGFR1 signaling functions during progenitor differentiation, FGFR1 has an FGF20-independent, Sox2-dependent role in specification. We also show that a combination of reduction in Sox2 expression and Fgf20 deletion recapitulates the Fgfr1-deletion phenotype. Furthermore, we uncovered a strong genetic interaction between Sox2 and Fgf20, especially in regulating the development of hair cells and supporting cells towards the basal end and the outer compartment of the organ of Corti. To explain this genetic interaction and its effects on the basal end of the organ of Corti, we provide evidence that decreased Sox2 expression delays specification, which begins at the organ of Corti apex, while Fgf20-deletion results in premature onset of differentiation, which begins near the organ of Corti base. Thereby, Sox2 and Fgf20 interact to ensure that specification occurs before differentiation towards the cochlear base. These findings reveal an intricate developmental program regulating organ of Corti development along the basal-apical axis of the cochlea.Author summaryThe mammalian cochlea contains the organ of Corti, a specialized sensory epithelium populated by hair cells and supporting cells that detect sound. Hair cells are susceptible to injury by noise, toxins, and other insults. In mammals, hair cells cannot be regenerated after injury, resulting in permanent hearing loss. Understanding genetic pathways that regulate hair cell development in the mammalian organ of Corti will help in developing methods to regenerate hair cells to treat hearing loss. Many genes are essential for hair cell and supporting cell development in the mouse organ of Corti. Among these are Sox2, Fgfr1, and Fgf20. Here, we investigate the relationship between these three genes to further define their roles in development.Interestingly, we found that Sox2 and Fgf20 interact to affect hair cell and supporting cell development in a spatially-graded manner. We found that cells toward the outer compartment and the base of the organ of Corti are more strongly affected by the loss of Sox2 and Fgf20. We provide evidence that this spatially-graded effect can be partially explained by the roles of the two genes in the precise timing of two sequential stages of organ of Corti development, specification and differentation.


Author(s):  
Martin A. Estermann ◽  
Mylene M. Mariette ◽  
Julie L. M. Moreau ◽  
Alexander N. Combes ◽  
Craig A. Smith

During embryonic gonadal development, the supporting cell lineage is the first cell type to differentiate, giving rise to Sertoli cells in the testis and pre-granulosa cells in the ovary. These cells are thought to direct other gonadal cell lineages down the testis or ovarian pathways, including the germline. Recent research has shown that, in contrast to mouse, chicken gonadal supporting cells derive from a PAX2/OSR1/DMRT1/WNT4 positive mesenchymal cell population. These cells colonize the undifferentiated genital ridge during early gonadogenesis, around the time that germ cells migrate into the gonad. During the process of somatic gonadal sex differentiation, PAX2 expression is down-regulated in embryonic chicken gonads just prior to up-regulation of testis- and ovary-specific markers and prior to germ cell differentiation. Most research on avian gonadal development has focused on the chicken model, and related species from the Galloanserae clade. There is a lack of knowledge on gonadal sex differentiation in other avian lineages. Comparative analysis in birds is required to fully understand the mechanisms of avian sex determination and gonadal differentiation. Here we report the first comparative molecular characterization of gonadal supporting cell differentiation in birds from each of the three main clades, Galloanserae (chicken and quail), Neoaves (zebra finch) and Palaeognathe (emu). Our analysis reveals conservation of PAX2+ expression and a mesenchymal origin of supporting cells in each clade. Moreover, down-regulation of PAX2 expression precisely defines the onset of gonadal sex differentiation in each species. Altogether, these results indicate that gonadal morphogenesis is conserved among the major bird clades.


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