scholarly journals Author response: Timing mechanism of sexually dimorphic nervous system differentiation

2018 ◽  
Author(s):  
Laura Pereira ◽  
Florian Aeschimann ◽  
Chen Wang ◽  
Hannah Lawson ◽  
Esther Serrano-Saiz ◽  
...  
2020 ◽  
Author(s):  
Emily A Bayer ◽  
Rebecca C Stecky ◽  
Lauren Neal ◽  
Phinikoula S Katsamba ◽  
Goran Ahlsen ◽  
...  

2020 ◽  
Author(s):  
Dunja D. Bijelić ◽  
Katarina D. Milićević ◽  
Milica N. Lazarević ◽  
Djordje M. Miljković ◽  
Jelena J. Bogdanović Pristov ◽  
...  

2020 ◽  
Vol 21 (23) ◽  
pp. 9000
Author(s):  
Eva Falvo ◽  
Silvia Diviccaro ◽  
Roberto Cosimo Melcangi ◽  
Silvia Giatti

Peripheral neuropathy (PN) refers to many conditions involving damage to the peripheral nervous system (PNS). Usually, PN causes weakness, numbness and pain and is the result of traumatic injuries, infections, metabolic problems, inherited causes, or exposure to chemicals. Despite the high prevalence of PN, available treatments are still unsatisfactory. Neuroactive steroids (i.e., steroid hormones synthesized by peripheral glands as well as steroids directly synthesized in the nervous system) represent important physiological regulators of PNS functionality. Data obtained so far and here discussed, indeed show that in several experimental models of PN the levels of neuroactive steroids are affected by the pathology and that treatment with these molecules is able to exert protective effects on several PN features, including neuropathic pain. Of note, the observations that neuroactive steroid levels are sexually dimorphic not only in physiological status but also in PN, associated with the finding that PN show sex dimorphic manifestations, may suggest the possibility of a sex specific therapy based on neuroactive steroids.


Author(s):  
Julia Patzig ◽  
Michelle S Erwig ◽  
Stefan Tenzer ◽  
Kathrin Kusch ◽  
Payam Dibaj ◽  
...  

2016 ◽  
Vol 18 (4) ◽  
pp. 415-424 ◽  

One of the most sexually dimorphic aspects of metabolic regulation is the bidirectional modulation of glucose and energy homeostasis by testosterone in males and females. Testosterone deficiency predisposes men to metabolic dysfunction, with excess adiposity, insulin resistance, and type 2 diabetes, whereas androgen excess predisposes women to insulin resistance, adiposity, and type 2 diabetes. This review discusses how testosterone acts in the central nervous system, and especially the hypothalamus, to promote metabolic homeostasis or dysfunction in a sexually dimorphic manner. We compare the organizational actions of testosterone, which program the hypothalamic control of metabolic homeostasis during development, and the activational actions of testosterone, which affect metabolic function after puberty. We also discuss how the metabolic effect of testosterone is centrally mediated via the androgen receptor.


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