Histogenesis of the deep cerebellar nuclei in the mouse: an autoradiographic study

Pierce, Elizabeth Taber

doi:10.1016/0006-8993(75)90124-9

Cited by 53 publications

(27 citation statements)

References 11 publications

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“…This interpretation fits very well with the studies of Altman and Bayer (1985c); earlier migrations of Purkinje cells might be radial, and potentially unaffected by GIRK2, whereas later migrations might follow a course similar to that of the migrating DCN neurons and therefore be indistinguishable from them as judged by anatomical observations. Consistent with this idea, the later-born Purkinje cells and DCN neurons are found to populate more medial regions of the cerebellum (Taber Pierce, 1975;Altman and Bayer, 1985c).…”

Section: Implications For Normal Cerebellar Developmentsupporting

confidence: 55%

“…Expression of girk2 in the developing neurons of the DCN has not been reported specifically, probably because of the difficulty of unequivocally identifying these neurons at embryonic time points. girk2 is expressed throughout the developing cerebellar anlage at E14.5 (Slesinger et al, 1996), at which time all DCN neurons are postmitotic and migratory (Taber Pierce, 1975).…”

Section: An Expanded Model Of the Weaver Mutationmentioning

confidence: 99%

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Failed Cell Migration and Death of Purkinje Cells and Deep Nuclear Neurons in theweaverCerebellum

et al. 1997

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The mouse neurological mutant weaver has an atrophic cerebellar cortex with deficits in both Purkinje and granule cell number. Although granule cells are known to die postnatally shortly after their final cell division, the cause of the Purkinje cell deficit (cell death vs lack of production) is unknown. We report here a quantitative analysis of large cerebellar neurons of the weaver mutant during postnatal development. We explored the hypothesis that the cells of the entire cerebellar anlage were affected by the mutation by including in our study the neurons of the deep cerebellar nuclei (DCN). Our analysis reveals that in homozygous weaver mutants (1) the DCN are displaced laterally, display an abnormal anatomy, and suffer a 20 -25% decrease in neuron number; (2) this numerical deficit is located in medial regions, similar to the localization of cortical deficits in both Purkinje and granule cells; (3) pyknotic figures are present in the juvenile DCN and in the Purkinje cell layer; and (4) the majority of cell death in these populations occurs not in medial regions where the numerical deficits are observed, but rather laterally where adult cell number is nearly normal. These results lead us to propose that the complete weaver phenotype includes a failure of the cell movements that lead to the fusion of the bilateral cerebellar anlage, and that this failure to migrate properly leaves some of the Purkinje cells and DCN neurons in a position where they are unable to make appropriate connections, leading to their death. In addition to implications for normal development, these observations suggest that weaver effects on the cerebellum can be unified into one consolidated model in which failure of cell movement affects all major cerebellar neurons.

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Section: Implications For Normal Cerebellar Developmentsupporting

confidence: 55%

Section: An Expanded Model Of the Weaver Mutationmentioning

confidence: 99%

Failed Cell Migration and Death of Purkinje Cells and Deep Nuclear Neurons in theweaverCerebellum

et al. 1997

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“…1A, 6A). The path and time course of this migration are similar to that forming the deep cerebellar nuclei (Pierce, 1975;Altman and Bayer, 1985a,b), suggesting that the tract is the superior cerebellar peduncle. The deep cerebellar nuclei, however, are a mix of stained and unstained cells, and the r1 WL migration contributes predominantly to the fastigial and intermediate nuclei (Figs.…”

Section: Rhombomere 1 (Cerebellum/isthmus)mentioning

confidence: 59%

“…An extensive literature describes the rhombic lip origins and migrations of the hindbrain neural crest (e.g., Nichols, 1981Nichols, , 1987Tan and Morris-Kay, 1985;Trainor et al, 2002). The rhombic lip and the hindbrain cell populations that migrate from it have been examined using classic morphological stains (see Essick, 1912), experimental manipulation (Harkmark, 1954;Tan and LeDouarin, 1991), autoradiography (Miale and Sidman, 1961;Pierce, 1966Pierce, , 1967Pierce, , 1973Pierce, , 1975Altman and Bayer, 1987a-d), dye lineage tracing (Wingate and Hatten, 1999), viral cell lineage tracing (Lin et al, 2001), and conditional gene expression lineage tracing (Rodriguez and Dymecki, 2000;Fü nfschilling and Reichardt, 2002). In addition, some insights into the genetic regulation of the lip have been gathered Wingate, 2001).…”

Section: Introductionmentioning

confidence: 99%

Migratory routes and fates of cells transcribing the Wnt‐1 gene in the murine hindbrain

Nichols

Bruce

2005

Developmental Dynamics

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“…Classical 3 H-birthdating studies (Pierce, 1975) provide evidence that cells born in this period are progenitors of the cerebellar nuclei. To confirm the identity of this progenitor cell population, we performed BrdU labeling experiments in combination with immunolocalization of MEIS2.…”

Section: Resultsmentioning

confidence: 99%

Molecular Markers of Neuronal Progenitors in the Embryonic Cerebellar Anlage

Morales¹,

Hatten²

2006

J. Neurosci.

160

158

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The cerebellum, like the cerebrum, includes a nuclear structure and an overlying cortical structure. Experiments in the past decade have expanded knowledge beyond the traditional function of the cerebellum to include critical roles in motor learning and memory and sensory discrimination. The initial steps in cerebellar development depend on inductive signaling involving FGF and Wnt proteins produced at the mesencephalic/metencephalic boundary. To address the issue of how individual cerebellar cell fates within the cerebellar territory are specified, we examined the expression of transcription factors, including mammalian homologues of LIM homeodomaincontaining proteins, basic helix-loop-helix proteins, and three amino acid loop-containing proteins. The results of these studies show that combinatorial codes of transcription factors define precursors of the cerebellar nuclei, and both Purkinje cells and granule neurons of the cerebellar cortex. Examination of gene expression patterns in several hundred lines of Egfp-BAC (bacterial artificial chromosome) transgenic mice in the GENSAT Project revealed numerous genes with restricted expression in cerebellar progenitor populations, including genes specific for cerebellar nuclear precursors and Purkinje cell precursors. In addition, we identified patterns of gene expression that link granule and Purkinje cells to their precerebellar nuclei. These results identify molecular pathways that offer new insights on the development of the nuclear and cortical structures of the cerebellum, as well as components of the cerebellar circuitry.

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Histogenesis of the deep cerebellar nuclei in the mouse: an autoradiographic study

Cited by 53 publications

References 11 publications

Failed Cell Migration and Death of Purkinje Cells and Deep Nuclear Neurons in theweaverCerebellum

Failed Cell Migration and Death of Purkinje Cells and Deep Nuclear Neurons in theweaverCerebellum

Migratory routes and fates of cells transcribing the Wnt‐1 gene in the murine hindbrain

Molecular Markers of Neuronal Progenitors in the Embryonic Cerebellar Anlage

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