Sex differences in cell migration in the preoptic area/anterior hypothalamus of mice

Henderson, Rachel G.; Brown, Alison E; Tobet, Stuart A.

doi:10.1002/(sici)1097-4695(19991105)41:2<252::aid-neu8>3.0.co;2-w

Cited by 60 publications

(42 citation statements)

References 61 publications

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“…Clonal analyses of the avian ventral forebrain [53] and the distribution of specific hypothalamic neurons at different developmental stages in the rat [52] provided confirmatory evidence, although other diencephalic areas show some widely dispersed clones [54,55]. In addition, intrahypothalamic tangential migration as well as migration from the olfactory placode, telencephalon and diencephalon into the hypothalamus have been described [44,56-58]. Here we show that the progenitor domains coincide with the regions where the Shh-derived cells settle, suggesting little or no mixing of cells belonging to different domains.…”

Section: Discussionmentioning

confidence: 99%

“…Obviously, the simple longitudinal versus transverse subdivision that works so well in the spinal cord breaks down in the hypothalamus and telencephalon; therefore, it might be time to redefine a novel dorsal subdivision ventral to the telencephalon. Furthermore, it remains to be investigated which hypothalamic neurons originate in the telencephalon [56,64,65] and whether they preserve any anatomical or functional links with their region of origin.…”

Section: Discussionmentioning

confidence: 99%

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Sonic hedgehog lineage in the mouse hypothalamus: from progenitor domains to hypothalamic regions

2012

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BackgroundThe hypothalamus is a brain region with essential functions for homeostasis and energy metabolism, and alterations of its development can contribute to pathological conditions in the adult, like hypertension, diabetes or obesity. However, due to the anatomical complexity of the hypothalamus, its development is not well understood. Sonic hedgehog (Shh) is a key developmental regulator gene expressed in a dynamic pattern in hypothalamic progenitor cells. To obtain insight into hypothalamic organization, we used genetic inducible fate mapping (GIFM) to map the lineages derived from Shh-expressing progenitor domains onto the four rostrocaudally arranged hypothalamic regions: preoptic, anterior, tuberal and mammillary.ResultsShh-expressing progenitors labeled at an early stage (before embryonic day (E)9.5) contribute neurons and astrocytes to a large caudal area including the mammillary and posterior tuberal regions as well as tanycytes (specialized median eminence glia). Progenitors labeled at later stages (after E9.5) give rise to neurons and astrocytes of the entire tuberal region and in particular the ventromedial nucleus, but not to cells in the mammillary region and median eminence. At this stage, an additional Shh-expressing domain appears in the preoptic area and contributes mostly astrocytes to the hypothalamus. Shh-expressing progenitors do not contribute to the anterior region at any stage. Finally, we show a gradual shift from neurogenesis to gliogenesis, so that progenitors expressing Shh after E12.5 generate almost exclusively hypothalamic astrocytes.ConclusionsWe define a fate map of the hypothalamus, based on the dynamic expression of Shh in the hypothalamic progenitor zones. We provide evidence that the large neurogenic Shh-expressing progenitor domains of the ventral diencephalon are continuous with those of the midbrain. We demonstrate that the four classical transverse zones of the hypothalamus have clearly defined progenitor domains and that there is little or no cell mixing between the tuberal and anterior or the preoptic and anterior hypothalamus. Finally, we show that, in the tuberal hypothalamus, neurons destined for every mediolateral level are produced during a period of days, in conflict with the current 'three-wave' model of hypothalamic neurogenesis. Our work sets the stage for a deeper developmental analysis of this complex and important brain region.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Sonic hedgehog lineage in the mouse hypothalamus: from progenitor domains to hypothalamic regions

2012

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“…Previous studies examining the birthdate of cells comprising the SDN-POA of rats have not found evidence for a sex difference in neurogenesis [11,34,43,44]. A sex difference in the migration or aggregation of cells into the nucleus is possible, especially in light of work demonstrating effects of sex and estradiol on cell migration in embryonic slice cultures of the POA [45,46]. We note, however, that if differences in the migration or aggregation of cells account for sexual differentiation of the CALB-SDN, calbindin-ir cells in females must end up quite a distance away from the cluster seen in males (that is, beyond the boundaries of the grid used for counts here).…”

Section: Discussionmentioning

confidence: 99%

Effects of blocking developmental cell death on sexually dimorphic calbindin cell groups in the preoptic area and bed nucleus of the stria terminalis

2012

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BackgroundCalbindin-D28 has been used as a marker for the sexually dimorphic nucleus of the preoptic area (SDN-POA). Males have a distinct cluster of calbindin-immunoreactive (ir) cells in the medial preoptic area (CALB-SDN) that is reduced or absent in females. However, it is not clear whether the sex difference is due to the absolute number of calbindin-ir cells or to cell position (that is, spread), and the cellular mechanisms underlying the sex difference are not known. We examined the number of cells in the CALB-SDN and surrounding regions of C57Bl/6 mice and used mice lacking the pro-death gene, Bax, to test the hypothesis that observed sex differences are due to cell death.MethodsExperiment 1 compared the number of cells in the CALB-SDN and surrounding regions in adult males, females, and females injected with estradiol benzoate on the day of birth. In experiment 2, cell number in the CALB-SDN and adjacent regions were compared in wild-type and Bax knockout mice of both sexes. In addition, calbindin-ir cells were quantified within the principal nucleus of the bed nucleus of the stria terminalis (BNSTp), a nearby region that is larger in males due to Bax-dependent cell death.ResultsMales had more cells in the CALB-SDN as well as in surrounding regions than did females, and estradiol treatment of females at birth masculinized both measures. Bax deletion had no effect on cell number in the CALB-SDN or surrounding regions but increased calbindin-ir cell number in the BNSTp.ConclusionsThe sex difference in the CALB-SDN of mice results from an estrogen-dependent difference in cell number with no evidence found for greater spread of cells in females. Blocking Bax-dependent cell death does not prevent sex differences in calbindin-ir cell number in the BNST or CALB-SDN but increases calbindin-ir cell number in the BNSTp of both sexes.

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“…For example, as a result of the early hormonal surge the sexually dimorphic nucleus of the preoptic area (POA) is several times larger in males than in females (28), and the density of dendritic spine synapses on POA neurons is greater (29). The POA is a boundary structure that develops from cells migrating from both the classic diencephalic and telencephalic compartments (82). It is treated as a diencephalic structure in this paper due to its similarity in function and hormonal response to other hypothalamic structures.…”

Section: Introduction To Neuroendocrinologymentioning

confidence: 99%

Steroids, sex and the cerebellar cortex: implications for human disease

Dean

McCarthy

2008

Cerebellum

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Neurosteroids play an important role in the development of the cerebellum. In particular, estradiol and progesterone appear capable of inducing increases in dendritic spine density during development, and there is evidence that both are synthesized de novo in the cerebellum during critical developmental periods. In normal neonates and adults, there are few differences in the cerebellum between the sexes and most studies indicate that hormone and receptor levels also do not differ significantly during development. However, the sexes do differ significantly in risk of neuropsychological diseases associated with cerebellar pathology, and in animal models there are noticeable sex differences in the response to insult and genetic mutation. In both humans and animals, males tend to fare worse. Boys are more at risk for autism and Attention Deficit Hyperactivity Disorder than girls, and schizophrenia manifests at an earlier age in men. In rats males fare worse than females after perinatal exposure to polychlorinated biphenyls, and male mice heterozygous for the staggerer and reeler mutation show a more severe phenotype. Although very recent evidence suggests that differences in neurosteroid levels between the sexes in diseased animals may play a role in generating different disease phenotypes, the reason this hormonal difference occurs in diseased but not normal animals is currently unknown.

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Sex differences in cell migration in the preoptic area/anterior hypothalamus of mice

Cited by 60 publications

References 61 publications

Sonic hedgehog lineage in the mouse hypothalamus: from progenitor domains to hypothalamic regions

Sonic hedgehog lineage in the mouse hypothalamus: from progenitor domains to hypothalamic regions

Effects of blocking developmental cell death on sexually dimorphic calbindin cell groups in the preoptic area and bed nucleus of the stria terminalis

Steroids, sex and the cerebellar cortex: implications for human disease

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