Evidence map›Paper›PMID 19207822›Full record

ReviewJournal of neuroendocrinology2009

Control of cell number in the sexually dimorphic brain and spinal cord.

N G Forger

Open access · greenAbstract readReview
In one paragraph

Review in Journal of neuroendocrinology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed
12.0field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

51 citing papers in PubMed, 96 citations in OpenAlex.

  1. Article
  2. Article
  3. Microglia phagocytosis mediates the volume and function of the rat sexually dimorphic nucleus of the preoptic area.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  4. Deficiency in the cell-adhesion moleculeFrontiers in cell and developmental biology · 2023
    Article
  5. Article
  6. Exposure to prenatal PCBs shifts the timing of neurogenesis in the hypothalamus of developing rats.Journal of experimental zoology. Part A, Ecological and integrative physiology · 2020
    Article
  7. A new view of sexual differentiation of mammalian brain.Journal of comparative physiology. A, Neuroethology, sensory, neural, and behavioral physiology · 2020
    Review
  8. Review
  9. Rethinking sex determination of non-gonadal tissues.Current topics in developmental biology · 2019
    Review
  10. Article
  11. Article
  12. Review
  13. Review
  14. Article
  15. Article
  16. Patterns of cell death in the perinatal mouse forebrain.The Journal of comparative neurology · 2017
    Article
  17. Review
  18. Review
  19. Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

1 author at 1 institution in 1 country.

N G ForgerDepartment of Psychology and Center for Neuroendocrine Studies, University of Massachusetts, Amherst, MA 01003, USA. nforger@psych.umass.edu
University of Massachusetts Amherst · US

Funding

Cell Death and Neural Sex DifferencesR01MH068482 · NIMH · UNIVERSITY OF MASSACHUSETTS AMHERST · PI FORGER, NANCY G · 2004 to 2013
$2.9M
Sexual Differentiation of the Nervous SystemK02MH072825 · NIMH · UNIVERSITY OF MASSACHUSETTS AMHERST · PI FORGER, NANCY G · 2005 to 2009
$626k
NIMH NIH HHS K02 MH072825NIMH NIH HHS R01 MH068482
6 · The paper itself

Abstract

The hormonal control of cell death is currently the best-established mechanism for creating sex differences in cell number in the brain and spinal cord. For example, males have more cells than do females in the principal nucleus of the bed nucleus of the stria terminalis (BNSTp) and spinal nucleus of the bulbocavernosus (SNB), whereas females have a cell number advantage in the anteroventral periventricular nucleus (AVPV). In each case, the difference in cell number in adulthood correlates with a sex difference in the number of dying cells at some point in development. Mice with over- or under-expression of cell death genes have been used to test more directly the contribution of cell death to neural sex differences, to identify molecular mechanisms involved, and to determine the behavioural consequences of suppressing developmental cell death. Bax is a pro-death gene of the Bcl-2 family that is singularly important for apoptosis in neural development. In mice lacking bax, the number of cells in the BNSTp, SNB and AVPV are significantly increased, and sex differences in total cell number in each of these regions are eliminated. Cells rescued by bax gene deletion in the BNSTp express markers of differentiated neurones and the androgen receptor. On the other hand, sex differences in other phenotypically identified populations, such as vasopressin-expressing neurones in the BNSTp or dopaminergic neurones in AVPV, are not affected by either bax deletion or bcl-2 over-expression. Possible mechanisms by which testosterone may regulate cell death in the nervous system are discussed, as are the behavioural effects of eliminating sex differences in neuronal cell number.

Indexed as

Sex CharacteristicsAnimalsApoptosisbcl-2-Associated X ProteinBrainCell CountCell DeathDopamineFemaleGonadal Steroid HormonesHumansMaleNeuronsProto-Oncogene Proteins c-bcl-2Receptors, AndrogenSpinal Cordbcl-2-Associated X ProteinDopamineGonadal Steroid HormonesProto-Oncogene Proteins c-bcl-2Receptors, AndrogenVasopressins

Identifiers

PMID19207822
PMCPMC2683584
OpenAlexW2048118074

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.