broken gradient concentration theory cAMP ( for PSSD )
firstly, let me say thank you DrPowers for all the work you are doing for PFS and PSSD community. As a PSSD sufferer i appreciate it. This thing has ruined my life, but i am fighting.
I've spent recent few days studying your posts on PFS and PSSD mechanisms you are proposing or thinking of.
my background is mathematics, not biology/medicine so maybe im connecting the dots, maybe not but please hear me out everyone.
here is a wild guess :
SSRI use - > cellurar transporter ABCC5 is blocked -> gradient is damaged ( but we dont know how, maybe cAMP lvl is flatlined, maybe cell is oversaturated with metabolic waste ) -> no signal -> system stuck in bad equilibirum -> numbness, anhedonia, genital anasthesia
so i read that you have some initial success with roflumilast ( pde4 inhibitor ) but you are unsure if thats a window or permanent improvement
so what do you think about this strategy ?
perhaps this signalling mechanism is stuck in a scenario optimized for high stimulus, which is no longer there, after stopping SSRI use, or just from adaptation
instead of shocking a system with surge ( like giving PDE4 ) , lets starve it with use of sertonin and dopamine receptor antagonists , we block signals, we trick cells to thinking there is sensory deprivation, mechanism has to upregulate
how to do it ? 5ht1a receptor antagonist. i think it worked with rats, but assumed mechanism of action was different. https://pubmed.ncbi.nlm.nih.gov/19435548/
kind regards and all the best in your work !
u/drWillPowers