Can Gonadal Steroids Influence Cell Position in the Developing Brain?

Tobet, Stuart A.; Chickering, Troy W.; Hanna, Iris K.; Crandall, James E.; Schwarting, Gerald A.

doi:10.1006/hbeh.1994.1028

Cited by 32 publications

(29 citation statements)

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“…We did not rule out the presence of noncholinergic neurons within our cultures, so we cannot exclude the possibility that the effects of E 2 on VAChT-IR elements are mediated indirectly. In addition, astrocytes, which modulate neuronal activity (Theodosis and Poulain, 1999), are also a target of E 2 (Garcia-Segura et al, 1989;Tobet et al, 1994) and contain E 2 receptors (Hosli et al, 2001). Surprisingly, in contrast to the proliferative and MAPK-stimulating effects of E 2 in neurons, Zhang et al (2002) observed that E 2 decreased cell proliferation in astrocytes, associated with downregulated ERK1/2, and increased cell death.…”

Section: Is the Effect Of Estrogen Direct Or Mediated?mentioning

confidence: 99%

Morphological Effects of Estrogen on Cholinergic NeuronsIn VitroInvolves Activation of Extracellular Signal-Regulated Kinases

Dominguez¹,

Jalali²,

Lacalle³

2004

J. Neurosci.

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In the present study, we examined the ability of estrogen to enhance cholinergic neurite arborization in vitro and identified the signal transduction cascade associated with this effect. Basal forebrain primordia collected from rat pups on postnatal day 1 were cultured for 2 weeks and then treated with 5 nM 17␤-estradiol for 24 hr. Cholinergic neurons were identified immunocytochemically with an antibody against the vesicular acetylcholine transporter and digitally photographed. Morphological analysis indicated that female cultures respond to estrogen treatment with an increase in total neurite length per neuron (4.5-fold over untreated controls) and in total branch segment number per neuron (2.3-fold over controls). In contrast, there was no change in total neurite length per neuron in male cultures, and we also observed a decrease in total branch segment number per neuron (0.5-fold below controls). Detailed histograms indicated that estrogen increases primary and secondary branch length and number and also increases terminal neuritic branches to the seventh order in female cultures. In a second set of experiments, we investigated the signal transduction cascade involved in this response, and found that an upstream extracellular signal-regulated kinase (ERK) inhibitor blocked the ability of estrogen to enhance outgrowth in female cultures. Our study provides strong evidence in support of the fact that the ERK pathway is required for estrogen-induced structural plasticity in the cholinergic system of female rats. Understanding the intracellular processes that underlie the response of cholinergic neurons to estrogen provides a necessary step in elucidating how cholinergic neurons can be particularly susceptible to degeneration in postmenopausal women.

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Section: Is the Effect Of Estrogen Direct Or Mediated?mentioning

confidence: 99%

Morphological Effects of Estrogen on Cholinergic NeuronsIn VitroInvolves Activation of Extracellular Signal-Regulated Kinases

Dominguez¹,

Jalali²,

Lacalle³

2004

J. Neurosci.

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“…One possible reason for this discrepancy in number is that the residual expression of Dlx still allows some interneurons to differentiate and to migrate to the pallium. To determine if this was the case, we analyzed cell migration in organotypic slice cultures (Tobet et al, 1994), placing DiI crystals in the MGE at E13.5 and culturing the slices for 2 days. As shown in Fig.…”

Section: The Cerebral Cortex Of Vax1 -/-Mice Is Severely Depleted Of mentioning

confidence: 99%

“…Organotypic slice cultures were performed as described (Lavdas et al, 1999;Tobet et al, 1994). To examine the migratory pathways of neurons generated in septum or MGE, we placed small crystals of 1-1′-dyoctodecyl-3-3-3′-3′ tetramethylindocarbocyanine (DiI, Molecular Probes, Eugene OR) in the region of interest.…”

Section: Organotypic Slice Culture Experimentsmentioning

confidence: 99%

“…We wanted to verify that the GABAergic cell migration from the septum was indeed missing in the Vax1 -/-brains. We cultured E13.5 brains from wild-type and Vax1 mutants in an organotypic culture assay (Tobet et al, 1994), implanting in the developing septal area a small piece of bamboo soaked in the fluorescent tracer DiI. Fig.…”

Section: The Septal Area Is Absent In Vax1 -/-Micementioning

confidence: 99%

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Compromised generation of GABAergic interneurons in the brains ofVax1-/- mice

et al. 2004

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The subcortical telencephalon is the major source of GABAergic interneurons that, during development, tangentially migrate to the cerebral cortex, where they modulate the glutamatergic excitatory action of pyramidal cells. The transcription factor Vax1, an intracellular mediator of both Shh and Fgf signaling, is expressed at high levels in the medial and lateral ganglionic eminences (MGE and LGE, respectively), in the septal area (SA), in the anterior entopeduncular area (AEP) and in the preoptic area (POA). We show that Vax1 expression in the neuroepithelium is graded: low in the ventricular zone (VZ) and high in the subventricular zone (SVZ), in a pattern that closely reproduces that of several members of the Dlx and Gsh family of homeobox transcription factors.We provide evidence that Vax1 plays an important role in proliferation and differentiation of MGE, POA/AEP and septum, and that the last structure is completely absent in Vax1 -/-mice. We show that the absence of Vax1 causes a severe depletion of GABAergic neurons in the neocortex, ranging from 30% to 44%, depending on the cortical areas considered. Taken together, our data indicate that a loss of function mutation in the Vax1 gene generates abnormalities in basal ganglia subventricular zone development and that it prevents the formation of the septum, impairing GABAergic interneuron generation.

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“…It has been demonstrated that aromatization of testosterone to estradiol in the brain plays an important role in mediating the effects of testosterone [3]. It is well known that estradiol affects many aspects of neuronal differentiation including apoptotic cell death [4], cell migration [5], synapse formation [6], and neurogenesis [7]. Most of these effects of estradiol occur through interactions with estrogen receptors, which serve as transcription factors for a wide variety of target genes [8].…”

mentioning

confidence: 99%

Expression Analyses of Sex Steroid-Regulated Genes in Neonatal Rat Hypothalamus

Yonehara

Suzuki

Yamanouchi

et al. 2003

Journal of Reproduction and Development

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Abstract.Estrogen plays an important role in sexual differentiation of the brain in rats during the perinatal period. To elucidate molecular mechanisms underlying sexual differentiation of the brain, in this study we investigated genes differentially expressed between sexes or induced to express by estrogen in neonatal rat hypothalamus using DNA microarray analysis in combination with real-time RT-PCR. It was found that the levels of expression of the genes encoding glutamic acid decarboxylase 65 and coronin 1b were higher in male than female hypothalamus on postnatal day (PN) 5 and those of collagen type 3 α1 and thioredoxin reductase 2 genes in female hypothalamus on PN5 were decreased and increased, respectively, by treatment with estradiol on PN2. Then the developmental changes in the expression of these 4 genes were examined from 1 day before the parturition to PN9, and they all showed sexual dimorphic patterns. In addition, dependence of the expression of these genes on either estradiol, testosterone or dihydrotestosterone during the neonatal period was confirmed. These results suggest that these four genes are involved in sexual differentiation of the rat brain, and that androgen per se as well as estrogen may take part in the processes. Key words: DNA microarray, Gene expression, Estrogen, Androgen, Sexual differentiation of brain (J. Reprod. Dev. 49: [547][548][549][550][551][552] 2003) exual differentiation of rat brain occurs during the perinatal period, i.e., around the day of birth to one week after birth, which is known as the critical period. In the male rat, testosterone secreted from the testis during the critical period induces the masculinization of the brain, while in the female, the absence of testosterone results in feminization of the brain [1,2]. It has been demonstrated that aromatization of testosterone to estradiol in the brain plays an important role in mediating the effects of testosterone [3]. It is well known that estradiol affects many aspects of neuronal differentiation including apoptotic cell death [4], cell migration [5], synapse formation [6], and neurogenesis [7]. Most of these effects of estradiol occur through interactions with estrogen receptors, which serve as transcription factors for a wide variety of target genes [8]. To elucidate the molecular mechanism of sexual differentiation of the brain, it is important to study signaling cascades regulated by estradiol during the critical period. In this context, we have previously identified the granulin precursor gene as an estradiol-as well as testosterone-inducible gene in the rat hypothalamus during the critical period [9][10][11].T e s t o s te r o n e c a n b e c o n v e r t e d t o 5α -dihydrotestosterone (DHT), a non-aromatizable androgen, by 5α-reductase in the neonatal brain [12], but the significance of androgen or androgen receptors in the sexual differentiation of the brain is

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Can Gonadal Steroids Influence Cell Position in the Developing Brain?

Cited by 32 publications

References 0 publications

Morphological Effects of Estrogen on Cholinergic NeuronsIn VitroInvolves Activation of Extracellular Signal-Regulated Kinases

Morphological Effects of Estrogen on Cholinergic NeuronsIn VitroInvolves Activation of Extracellular Signal-Regulated Kinases

Compromised generation of GABAergic interneurons in the brains ofVax1-/- mice

Expression Analyses of Sex Steroid-Regulated Genes in Neonatal Rat Hypothalamus

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