Equivalent ages in mouse and human embryos

Otis, Eileen M.; Brent, Robert L.

doi:10.1002/ar.1091200104

Cited by 193 publications

(82 citation statements)

References 23 publications

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“…Similarly, the duration of SCN cytogenesis in hamsters is 3 days (E10-E13) and is complete 3 days before birth. Based on comparative stages of development in humans and mice, human SCN cytogenesis is likely to occur during the 8 th week of gestation [24]. Not surprisingly, if the germinal epithelium of the third ventricle in mice is disrupted during the time of SCN cytogenesis, this leads to gross morphological disruptions of the nucleus and of circadian rhythms [29].…”

Section: Discussionmentioning

confidence: 99%

Development of the mouse suprachiasmatic nucleus: Determination of time of cell origin and spatial arrangements within the nucleus

Kabrita

Davis

2008

Brain Research

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The suprachiasmatic nucleus (SCN) in mammals functions as the principal circadian pacemaker synchronizing diverse physiological and behavioral processes to environmental stimuli. It consists of heterogeneous populations of cells with unique spatial organization that can vary among species, but are commonly discussed within a framework of two principal regions, the ventrolateral or dorsomedial halves of the nucleus or in other instances the core and shell. In both hamsters and rats, cells of different SCN regions have been shown to have different developmental histories. Using bromodeoxyuridine as a marker of cell division, the present study investigated the time of SCN cell origin in mice (C57BL/6) and their settling patterns within the nucleus. Results show that SCN cytogenesis occurs between embryonic days 12 and 15 and is complete 5 days prior to birth. Cells born on embryonic day 12 are mainly confined to a ventrolateral region of the mid-SCN, whereas cells produced later on embryonic days 13.5 and 14.5 form a cap around the cells produced first and extend into the posterior and anterior ends of the nucleus. These results suggest an ordered spatiotemporal program of SCN cytogenesis whereby a mid-SCN core is born first followed by a surrounding shell of later-born cells. Variation in cytogenesis could affect the relative sizes of different SCN regions and, thereby, affect its function. The relative contributions of a highly ordered program of cytogenesis and intercellular interactions after post-mitotic cells leave the germinal epithelium remain to be determined.

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Section: Discussionmentioning

confidence: 99%

Development of the mouse suprachiasmatic nucleus: Determination of time of cell origin and spatial arrangements within the nucleus

Kabrita

Davis

2008

Brain Research

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“…The newborn mouse is analogous to the human fetus in utero (Otis & Brent 1954). At birth, the mouse auditory system is immature and normal hearing thresholds take weeks to develop (e.g., Kasai et al 1981).…”

Section: Introductionmentioning

confidence: 99%

Cytomegalovirus (CMV) Infection Causes Degeneration of Cochlear Vasculature and Hearing Loss in a Mouse Model

Carraro

Almishaal

Hillas

et al. 2016

JARO

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Cytomegalovirus (CMV) infection is one of the most common causes of congenital hearing loss in children. We have used a murine model of CMV infection to reveal functional and structural cochlear pathogenesis. The cerebral cortex of Balb/c mice (Mus musculus) was inoculated with 2000 pfu (plaque forming units) of murine CMV on postnatal day 3. At 6 weeks of age, cochlear function was monitored using auditory brainstem response (ABR) and distortion product otoacoustic emission (DPOAE) measures. Histological assessment of cochlear vasculature using a corrosion cast technique was made at 8 weeks. Vascular casts of mCMV-damaged cochleas, and those of untreated control animals, were examined using scanning electron microscopy. We find very large variations in the degree of vascular damage in animals given identical viral injections (2000 pfu). The primary lesion caused by CMV infection is to the stria vascularis and to the adjacent spiral limbus capillary network. Capillary beds of the spiral ligament are generally less affected. The initial vascular damage is found in the mid-apical turn and appears to progress to more basal cochlear regions. After viral migration to the inner ear, the stria vascularis is the primary affected structure. We suggest that initial auditory threshold losses may relate to the poor development or maintenance of the endocochlear potential caused by strial dysfunction. Our increased understanding of the pathogenesis of CMV-related hearing loss is important for defining methods for early detection and treatment.

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“…The presomitic period ending at 21 days p.c. is longer than those observed in the guinea-pig (Scott, 1937), hamster (Boyer, 1953), mouse (Gruneberg, 1943) and Mongolian gerbil (Bagwell & Leavitt, 1974), but similar to that of the human Embryo (Otis & Brent, 1954).…”

Section: Discussionmentioning

confidence: 47%