T3 thyroid hormone transporter MCT8, histamine, dopamine & sexual behavior

In response to a post by oksana s on MedCram forum re: research she conducted on DKO mct8/oatp (AHDS) mice - females are reportedly androgenized and aggressive and selectively kill their own female pups. OS also noted an increase in sexual behavior just prior to symptom onset in SOD1 KO mice (ALS model) and reported the same in HD model mice.

Your mice reminded me of a news article I had read on sexual development & histamine signalling: https://www.sciencedaily.com/releases/2018/08/180814151001.htm

I searched and found this, published 2 yrs prior to the above [this site has some malware scripts on it for some reason, though it looks just to be an academic publishing site - I opened it in a container tab so I could read it]: https://clinical-and-molecular-endocrinology.imedpub.com/thyroid-hormone-derivatives-and-brain-histamine-what-should-we-expect.php?aid=17259

Do you think a histamine modulating drug given during pregnancy would normalize sexual behavior in the resulting pups?

Also wondering about the interactions with dopamine, especially with respect to what you note about the ALS mice. In HD, there's a biphasic alteration in dopaminergic neurotransmission: https://pubmed.ncbi.nlm.nih.gov/24968783/
In this article they discuss dopamine and excitotoxicity, but I wonder if there is more direct dopamine-induced toxicity from oxidized dopamine (and I think I read something the other day about nitrated dopamine, but am unable to find it - oh well, perhaps I imagined it).  
 
{ I meant nitrosylated and I did imagine it - however there are a whole slew of other proteins that can become s-nitrosylated and contribute to PD pathogenesis: 
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3712898/ 
 
Low levels of uric acid, the major peroxynitrite scavenger, are associated with PD and also low fat dairy intake, which lowers uric acid levels, is positively associated with PD risk and progression }
 

Allan-Herndon-Dudley syndrome

"An X-linked intellectual disability syndrome with neuromuscular involvement characterized by infantile hypotonia, muscular hypoplasia, spastic paraparesis with dystonic/athetoic movements, and severe cognitive deficiency.
AHDS is caused by mutations in the SLC16A2 gene (Xq13.2), which encodes for monocarboxylate transporter 8 (MCT8), a specific transporter for thyroid hormone T3. Identified mutations include truncations, in-frame deletions, nonsense and missense mutations. Neurological problems may be due to an inability to transport thyroid hormone T3 into some neuronal cells."


To read:

Thyroid Hormone, Thyroid Hormone Metabolites and Mast Cells: A Less Explored Issue [2019] - https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6449760/


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