Immunological Localization and Ontogenetic Development of Inhibin α Subunit in Rat Brain

Fujimura,; Ohsawa,; Funaba, Masayuki; Murata,; Takahashi, Daisuke; Abé,; Torii,

doi:10.1046/j.1365-2826.1999.00310.x

Cited by 11 publications

(6 citation statements)

References 2 publications

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“…Inhibin alpha subunit and activin expression and protein localization in different parts of the brain were shown in previous studies (Roberts et al., 1996; Fujimura et al., 1999). However, the exact function of this protein in the brain is unknown.…”

Section: Discussionsupporting

confidence: 71%

An association analysis at 2q36 reveals a new candidate susceptibility gene for juvenile absence epilepsy and/or absence seizures associated with generalized tonic-clonic seizures

et al. 2011

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Summary Purpose: To further evaluate the previously shown linkage of absence epilepsy (AE) to 2q36, both in human and WAG/Rij absence rat models, a 160‐kb region at 2q36 containing eight genes with expressions in the brain was targeted in a case–control association study involving 205 Turkish patients with AE and 219 controls. Methods: Haplotype block and case–control association analysis was carried out using HAPLOVIEW 4.0 and inhibin alpha subunit (INHA) gene analysis by DNA sequencing. Key Findings: An association was found between the G allele of rs7588807 located in the INHA gene and juvenile absence epilepsy (JAE) syndrome and patients having generalized tonic–clonic seizures (GTCS) with p‐values of 0.003 and 0.0002, respectively (uncorrected for multiple comparisons). DNA sequence analysis of the INHA gene in 110 JAE/GTCS patients revealed three point mutations with possible damaging effects on inhibin function in three patients and the presence of a common ACTC haplotype (H1) with a possible dominant protective role conferred by the T allele of rs7588807 with respective p‐values of 0.0005 and 0.0014. Significance: The preceding findings suggest that INHA could be a novel candidate susceptibility gene involved in the pathogenesis of JAE or AE associated with GTCS.

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Section: Discussionsupporting

confidence: 71%

An association analysis at 2q36 reveals a new candidate susceptibility gene for juvenile absence epilepsy and/or absence seizures associated with generalized tonic-clonic seizures

et al. 2011

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“…128 The inhibin a-subunit has been shown to be expressed in the hypothalamic arcuate nucleus, the hippocampal dentate gyrus, and the cerebral cortex of the rat brain. 133 The specific role of locally produced inhibin and follistatin in these regions of the brain is not known, but they may be responsible for modulating the effects of activin in the paracrine regulation of neuronal outputs. However, despite extensive in vitro evidence that activin can exert effects on GnRH release, in vivo experiments in ACT-RII receptor null mice demonstrated that although signaling through the ACT-RII receptor is critical for FSH homeostasis, it is not essential for GnRH biosynthesis or induction of pituitary GnRHR expression.…”

Section: Regulation Of Gnrh Secretion By Inhibin Activin and Follismentioning

confidence: 99%

Regulation of Gonadotropins by Inhibin and Activin

Gregory¹,

Kaiser²

2004

Semin Reprod Med

128

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Inhibin, activin, and follistatin were first identified as gonadal hormones that could exert selective effects on follicle-stimulating hormone (FSH) secretion without affecting luteinizing hormone (LH). Although the primary source of inhibin remains the gonad, both activin and follistatin are produced in extragonadal tissues and can exert effects on FSH through an autocrine-paracrine mechanism. These proteins can effect the regulation of the gonadotropins at many levels. First, activin can directly stimulate FSH biosynthesis and release from the gonadotrope cells of the pituitary gland. Second, activin up-regulates gonadotropin-releasing hormone receptor (GnRHR) gene expression, leading to alterations in the synthesis and release of both gonadotropins in response to GnRH. Third, activin can stimulate GnRH release from GnRH neurons in the hypothalamus and thereby affect FSH and LH secretion. Both inhibin and follistatin can negatively regulate these effects by preventing activin binding to the activin receptor at the cell membrane and blocking activation of downstream signal transduction pathways. This review concentrates on the mechanisms through which inhibin, activin, and follistatin regulate the gonadotropins. We discuss the expression of inhibin/activin subunits and receptors throughout the hypothalamus and pituitary and their role in the regulation of FSH and LH. The mechanisms of inhibin and activin signaling are also reported, with particular attention to developments in our understanding of inhibin receptor action and activin-induced transcriptional regulation of the FSHbeta gene promoter. Finally, we present recent findings that other members of the transforming growth factor beta superfamily may also play an important role in transcriptional regulation of the pituitary gonadotropins.

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“…Cks2 21 . Further, genes related to astrocytic development ( Inha and Bmp5 ) indicate an immature phenotype 22,23 . In line with this, the astrocytes attempt to restore the lack of neurons as indicated by increased levels of Neurod1 , which has been shown to be able to convert astrocytes to neurons 24 .…”

Section: Resultsmentioning

confidence: 99%

Chronic disturbance in the thalamus following cranial irradiation to the developing mouse brain

Boström

Eriksson

Danial

et al. 2019

Sci Rep

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Better survival rates among pediatric brain tumor patients have resulted in an increased awareness of late side effects that commonly appear following cancer treatment. Radiation-induced changes in hippocampus and white matter are well described, but do not explain the full range of neurological late effects in childhood cancer survivors. The aim of this study was to investigate thalamus following cranial irradiation (CIR) to the developing brain. At postnatal day 14, male mice pups received a single dose of 8 Gy CIR. Cellular effects in thalamus were assessed using immunohistochemistry 4 months after CIR. Interestingly, the density of neurons decreased with 35% ( p = 0.0431) and the density of astrocytes increased with 44% ( p = 0.011). To investigate thalamic astrocytes, S100β + cells were isolated by fluorescence-activated cell sorting and genetically profiled using next-generation sequencing. The phenotypical characterization indicated a disrupted function, such as downregulated microtubules’ function, higher metabolic activity, immature phenotype and degraded ECM. The current study provides novel insight into that thalamus, just like hippocampus and white matter, is severely affected by CIR. This knowledge is of importance to understand the late effects seen in pediatric brain tumor survivors and can be used to give them the best suitable care.

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Immunological Localization and Ontogenetic Development of Inhibin α Subunit in Rat Brain

Cited by 11 publications

References 2 publications

An association analysis at 2q36 reveals a new candidate susceptibility gene for juvenile absence epilepsy and/or absence seizures associated with generalized tonic-clonic seizures

An association analysis at 2q36 reveals a new candidate susceptibility gene for juvenile absence epilepsy and/or absence seizures associated with generalized tonic-clonic seizures

Regulation of Gonadotropins by Inhibin and Activin

Chronic disturbance in the thalamus following cranial irradiation to the developing mouse brain

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