Document Detail

Control of cell number in the sexually dimorphic brain and spinal cord.
MedLine Citation:
PMID:  19207822     Owner:  NLM     Status:  MEDLINE    
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.
N G Forger
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.; Review    
Journal Detail:
Title:  Journal of neuroendocrinology     Volume:  21     ISSN:  1365-2826     ISO Abbreviation:  J. Neuroendocrinol.     Publication Date:  2009 Mar 
Date Detail:
Created Date:  2009-04-14     Completed Date:  2009-08-10     Revised Date:  2014-09-19    
Medline Journal Info:
Nlm Unique ID:  8913461     Medline TA:  J Neuroendocrinol     Country:  England    
Other Details:
Languages:  eng     Pagination:  393-9     Citation Subset:  IM    
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Apoptosis / physiology
Brain / growth & development,  physiology*
Cell Count
Cell Death / physiology*
Dopamine / metabolism
Gonadal Steroid Hormones / metabolism
Neurons / physiology*
Proto-Oncogene Proteins c-bcl-2 / metabolism
Receptors, Androgen / metabolism
Sex Characteristics*
Spinal Cord / growth & development,  physiology*
Vasopressins / metabolism
bcl-2-Associated X Protein / metabolism
Grant Support
K02 MH072825/MH/NIMH NIH HHS; K02 MH072825/MH/NIMH NIH HHS; K02 MH072825-04/MH/NIMH NIH HHS; R01 MH068482/MH/NIMH NIH HHS; R01 MH068482/MH/NIMH NIH HHS; R01 MH068482-03/MH/NIMH NIH HHS; R01 MH068482-04/MH/NIMH NIH HHS
Reg. No./Substance:
0/Gonadal Steroid Hormones; 0/Proto-Oncogene Proteins c-bcl-2; 0/Receptors, Androgen; 0/bcl-2-Associated X Protein; 11000-17-2/Vasopressins; VTD58H1Z2X/Dopamine

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

Previous Document:  Neurobiological mechanisms underlying oestradiol negative and positive feedback regulation of gonado...
Next Document:  Role of the ventromedial hypothalamic orexin-1 receptors in regulation of gastric Acid secretion in ...