Regional Distribution of Sonic Hedgehog, Patched, and Smoothened mRNA in the Adult Rat Brain

Traiffort, Élisabeth; Charytoniuk, Dorota; Faure, Hélène; Ruat, Martial

doi:10.1046/j.1471-4159.1998.70031327.x

Cited by 115 publications

(91 citation statements)

References 21 publications

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“…It specifies the identity of different cell types in the ventral neural tube in early development (Pfaff and Kintner, 1998;Briscoe et al, 1999;Oppenheim et al, 1999). Although Shh is strong in inducing motor neurons from progenitor cells, there have been few reports characterizing its role in matured neurons (Miao et al, 1997;Traiffort et al, 1998Traiffort et al, , 1999Ho and Scott, 2002). This is the first evidence that nerve axotomy induces upregulation of both Shh and Smo.…”

Section: Discussionmentioning

confidence: 83%

The Upregulated Expression of Sonic Hedgehog in Motor Neurons after Rat Facial Nerve Axotomy

Akazawa¹,

Tsuzuki²,

Nakamura³

et al. 2004

J. Neurosci.

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Nerve injury leads to the induction of a large number of genes to repair the damage and to restore synaptic transmission. We have attempted to identify molecules whose mRNA expression is altered in response to facial nerve axotomy. Here we report that facial nerve axotomy upregulates Sonic hedgehog (Shh) and its receptor Smoothened (Smo) in facial motor neurons of adult rats, whereas facial nerve axotomy does not upregulate mRNA of Shh or Smo in neonatal rats. We tested whether overexpression of Shh in facial motor neurons of axotomized neonatal rats may promote neuronal survival. Adenovirus-mediated overexpression of Shh, but not that of ␤-galactosidase, transiently rescues axotomy-induced neuronal cell death for 3-5 d after axotomy. Finally, the pharmacological inhibitor of Shh signaling, cyclopamine, induces motor neuron death in adult rats after axotomy. These results suggest that Shh plays a regulatory role in nerve injury.

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Section: Discussionmentioning

confidence: 83%

The Upregulated Expression of Sonic Hedgehog in Motor Neurons after Rat Facial Nerve Axotomy

Akazawa¹,

Tsuzuki²,

Nakamura³

et al. 2004

J. Neurosci.

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“…Before Shh was shown to directly affect the BG population, Traifford et al [157] and Wallace [113] had already observed high expression levels of Ptch and Gli1 in small cells in the PCL, presumably in BGs, suggesting that Shh signaling pathway was active in these cells. Confirmation of a direct action of Shh came shortly later, when Dahmane and Ruiz-I-Altaba [95] first demonstrated the role of this ligand in BG differentiation, but, intriguingly, not in BG progenitor proliferation [95].…”

Section: Shh and Cerebellar Gliamentioning

confidence: 99%

Sonic hedgehog patterning during cerebellar development

Luca

Cerrato

Fucà

et al. 2015

Cell. Mol. Life Sci.

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Abstract:Robust evidence in literature indicates that the morphogenic factor Sonic Hedgehog (Shh) actively orchestrates several aspects of cerebellar development and maturation. During embryogenesis Shh signalling is active in the ventricular germinal zone (VZ) and represents an essential signal for proliferation of VZ-derived progenitors. Later, Purkinje cell (PC)-secreted Shh sustains the amplification of neurogenic niches active during postnatal development: the external granular layer (EGL) and the prospective white matter (PWM) where excitatory granule cells and inhibitory interneurons, respectively, are produced. In addition, Shh signalling acts on Bergmann glia differentiation and during development sustains cerebellar foliation. Here we review the most relevant functions of Shh during cerebellar ontogenesis, underlying the role of this ligand in the development of different cerebellar phenotypes. Keywords: Shh, mitogen, differentiation, cerebellum.Authors declare no conflict of interest. AbstractRobust evidence in literature indicates that the morphogenic factor Sonic Hedgehog (Shh) actively orchestrates several aspects of cerebellar development and maturation. During embryogenesis Shh

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“…However, particularly in the light of evidence that, late in gestation, Shh becomes expressed within the cortex itself (Traiffort et al, 1998;Dahmane et al, 2001), and that this expression is also eliminated in the NsCre:Shh Fl/Fl mutants (Fig. 7A), direct or secondary effects of Shh loss on cortical interneuron migration, differentiation or survival must also be considered.…”

Section: Reductions Of Somatostatin-and Parvalbuminexpressing Internementioning

confidence: 99%

Sonic hedgehog maintains the identity of cortical interneuron progenitors in the ventral telencephalon

2005

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Fate determination in the mammalian forebrain, where mature phenotypes are often not achieved until postnatal stages of development, has been an elusive topic of study despite its relevance to neuropsychiatric disease. In the ventral telencephalon, major subgroups of cerebral cortical interneurons originate in the medial ganglionic eminence (MGE), where the signaling molecule sonic hedgehog (Shh) continues to be expressed during the period of neuronogenesis. To examine whether Shh regulates cortical interneuron specification, we studied mice harboring conditional mutations in Shh within the neural tube. At embryonic day 12.5, NestinCre:ShhFl/Flmutants have a relatively normal index of S-phase cells in the MGE, but many of these cells do not co-express the interneuron fate-determining gene Nkx2.1. This effect is reproduced by inhibiting Shh signaling in slice cultures, and the effect can be rescued in NestinCre:ShhFl/Fl slices by the addition of exogenous Shh. By culturing MGE progenitors on a cortical feeder layer, cell fate analyses suggest that Shh signaling maintains Nkx2.1 expression and cortical interneuron fate determination by MGE progenitors. These results are corroborated by the examination of NestinCre:ShhFl/Fl cortex at postnatal day 12, in which there is a dramatic reduction in cell profiles that express somatostatin or parvalbumin. By contrast, analyses of Dlx5/6Cre:SmoothenedFl/Flmutant mice suggest that cell-autonomous hedgehog signaling is not crucial to the migration or differentiation of most cortical interneurons. These results combine in vitro and ex vivo analyses to link embryonic abnormalities in Shh signaling to postnatal alterations in cortical interneuron composition.

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Regional Distribution of Sonic Hedgehog, Patched, and Smoothened mRNA in the Adult Rat Brain

Cited by 115 publications

References 21 publications

The Upregulated Expression of Sonic Hedgehog in Motor Neurons after Rat Facial Nerve Axotomy

The Upregulated Expression of Sonic Hedgehog in Motor Neurons after Rat Facial Nerve Axotomy

Sonic hedgehog patterning during cerebellar development

Sonic hedgehog maintains the identity of cortical interneuron progenitors in the ventral telencephalon

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