Sex steroids and the development of the newborn mouse hypothalamus and preoptic area in vitro: III. Effects of estrogen on dendritic differentiation

Toran-Allerand, C. Dominique; Hashimoto, K; Greenough, William T.; Saltarelli, Maria Alessandra

doi:10.1016/0165-3806(83)90085-8

Cited by 121 publications

(31 citation statements)

References 19 publications

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“…In the same system, it has been demonstrated that the castration-induced decline in synaptic number is reversed by testosterone administration [33]. In vitro, administration of E promotes neurite outgrowth and dendritic differentiation in newborn mouse hypothalamic expiants [34,35] and in dissociated hypothalamic cells in the rat [36] and mouse [37]. In vivo, E administration has been shown to in crease the number of axo-dendritic synapses in the lateral sep tum [38] and the number of synapses in the midbrain central grey [39].…”

Section: Discussionmentioning

confidence: 95%

Gonadal Steroids Modify Dendritic Spine Density in Ventromedial Hypothalamic Neurons: A Golgi Study in the Adult Rat

et al. 1990

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Neurons in the adult rat ventromedial hypothalamic nucleus (VMN, 4–6 neurons per brain; 3–7 brains per group) were studied under various hormonal conditions using the single-section Golgi impregnation technique. Intact rats of both sexes and ovariectomized females treated with oil, estrogen or estrogen and progesterone were used. Golgi-impregnated neurons in the VMN were analyzed to determine possible differences in cell body size, number of primary dendrites, number of dendritic branchpoints and spine density. The only significant differences found were in spine density. In the VMN of ovariectomized rats given oil, there were significantly fewer spines on primary dendrites than in either estrogen-treated, estrogen plus progesterone-treated or intact female rats. There were no differences between intact male and female rats observed in any parameter. In addition, when spine density of VMN neurons was assessed throughout the estrous cycle, it was determined that spine density was significantly lower at diestrus than proestrus.

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Section: Discussionmentioning

confidence: 95%

Gonadal Steroids Modify Dendritic Spine Density in Ventromedial Hypothalamic Neurons: A Golgi Study in the Adult Rat

et al. 1990

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“…These data indicate that E2 concentrations observed in rodents and in women can serve a neuroprotective effect. In rats, neurotrophic (Toran-Allerand, 1976, 1980Faivre-Bauman et al, 1981;Nishizuka and Arai, 1981;Toran-Allerand et al, 1983;Morse et al, 1986;Wooley et al, 1990;Wooley and McEwen, 1992) and neuroprotective Singh et al, 1994;Behl et al, 1995;Goodman et al, 1996) effects of 17␤-E2 have been described. However, to our knowledge, 17␣-E2 has not been demonstrated previously to exert either neurotrophic or neuroprotective effects.…”

Section: Discussionmentioning

confidence: 99%

17α-Estradiol Exerts Neuroprotective Effects on SK-N-SH Cells

1997

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Estradiol (E2) has been shown to exert organizational, neurotrophic, and neuroprotective effects in the CNS. The present study assessed the specificity of the neuroprotective effects of estradiol for the potent 17␤-isomer. SK-N-SH cells from a human neuroblastoma cell line, which we have shown to be estrogen-responsive, were cultured at low or high plating density. Then cells were exposed to 17␤-E2 (0.2 or 2 nM), 17␣-E2 (0.2 or 2 nM), or cholesterol, testosterone, dihydrotestosterone, progesterone, or corticosterone (all at 2 nM). Cultures were insulted by serum deprivation, which caused a profound loss of cells. At 1 or 2 d of serum deprivation and steroid hormone replacement, the protection afforded cells by the steroid addition was assessed. Serum deprivation killed ϳ90% of cells cultured at both low and high plating density. Both 17␣-and 17␤-E2 provided protection of SK-N-SH cells at either plating density. Further, a 10-fold molar excess of tamoxifen antagonized only approximately one-third of the neuroprotective effects of either isomer of estradiol, and a 100-fold excess of tamoxifen had no additional effect on the neuroprotection by 17␤-E2. By contrast, none of the other steroids tested protected cells from the insult of serum deprivation. These results indicate that the neuroprotective effects of estrogens are not attributable to the general steroid structure, and the majority of the neuroprotection may not be mediated via a tamoxifenantagonized receptor mechanism.

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“…As a transcription factor, the ligand-activated ER is capable of regulating gene transcription by binding to specific DNA sequences (estrogen response elements) located in the 5) flanking regions of its target genes. Both in vivo and in vitro studies have documented the trophic influences of estrogen on promoting neurite outgrowth and differentiation [Toran-Allerand et al, 1983;Hammer and Jacobson, 1984;Gould et al, 1990]. The effects of estrogen on neuronal growth and differentiation may be mediated by direct activation of cytoskeletal and growthassociated genes [Ferreira and Caceres, 1991;Lustig et al, 1991].…”

Section: Potential Mechanisms Of Estrogen Action In the Zebra Finch Bmentioning

confidence: 99%

Developmental Regulation of the Distribution of Aromatase- and Estrogen-Receptor- mRNA-Expressing Cells in the Zebra Finch Brain

Jacobs¹,

Arnold

Campagnoni

1999

Dev Neurosci

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Strong evidence exists for the masculinizing effects of estrogen on the neural network that controls song learning and behavior in zebra finches. However, the mechanisms by which estrogen acts to influence the development of this circuitry are not well understood. In this study, we used in situ hybridization to detect the distribution of cells expressing mRNAs for AROM and ERα at postnatal days 5–25 (P5–25). Our findings revealed developmental regulation of both mRNAs in the neostriatum, archistriatum, hippocampus, diencephalon and midbrain. Within the vocal control circuitry, cells expressing ERα mRNA were found in the medial HVC (P10–25), archistriatum lateral to the RA (Ad; P25), in the ICo (P5–25), and along the fiber tract containing efferents from the RA. High levels of AROM mRNA were found in the neostriatum, including both the lateral and mMAN and along their projections to the RA and HVC, respectively, (P5–25), in the archistriatum (P18–25) and around RA (P18). Codistribution of the two mRNAs occurred along the border of the HVC suggesting that in this region, local synthesis of estrogen may be acting through its nuclear receptor to regulate gene transcription. Taken together, our findings show that the neural circuitry controlling song may be exposed to the effects of estrogen during early postnatal development. However, in most of the song control regions, these mRNAs were not expressed together either temporally or spatially, indicating that AROM may have a role in the development of the song system independent of ERα.

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Sex steroids and the development of the newborn mouse hypothalamus and preoptic area in vitro: III. Effects of estrogen on dendritic differentiation

Cited by 121 publications

References 19 publications

Gonadal Steroids Modify Dendritic Spine Density in Ventromedial Hypothalamic Neurons: A Golgi Study in the Adult Rat

Gonadal Steroids Modify Dendritic Spine Density in Ventromedial Hypothalamic Neurons: A Golgi Study in the Adult Rat

17α-Estradiol Exerts Neuroprotective Effects on SK-N-SH Cells

Developmental Regulation of the Distribution of Aromatase- and Estrogen-Receptor- mRNA-Expressing Cells in the Zebra Finch Brain

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