Spontaneous PM in Mice: the case for genetics

[webslave]

In a recent exchange I had with Dr Theoharides, I asked him if the studies he is aiming to do will look not only at whether stress causes mast cell degranulation in murine urogenital tissues (which I believe has already been shown), but also *how* this occurs. Dr Jerome Weiss postulates in this article: http://www.jmweissmd.com/article.htm that stress/anxiety causes a primitive tensing or clenching reaction in the pelvis. So I'd like to know if the mice are tensing their pelvic muscles, and thereby causing neuropathy, and hence irritating mast cells.

Dr Theo responded that they will induce inflammatory cystitis, with or without stress, in a variety of genetically deficient animals in order to identify the neurohormones involved.

So it looks as though nobody will be monitoring the pelvic muscles in these rodents, and that's a pity.

And there is another important question. It is possible to breed a type of rodent ("genetically deficient") that will get an inflamed bladder pretty reliably, without having to expose it to stress (like confinement in a tiny box where it cannot move - yes, cruel, I know).

But WHY do these specially bred rodents get inflamed bladders, or spontaneous CPPS/PM? Is it only because they have a genetic weakness that makes them get it, no matter what? Or is it because they are very nervy, anxious rodents that experience high anxiety and stress just by being alive, tensing their tiny little mousy pelvic muscles as they go?

And lastly, they may have inflammation in their urogenital tracts, but are they experiencing pain? Is someone looking at their brain patterns to see if the pain centres are stimulated?

A lot of questions, and maybe $1M is not enough to answer them all ...

[dshoskes]

A fundamental flaw of the animal models for "prostatitis" and IC is that they are models of urinary tract inflammation which can occur independently from pelvic pain and can be absent in pelvic pain. The "autoimmune prostatitis" models are really just models of category IV prostatitis which in the vast majority of humans is asymptomatic. While I have done rodent research to answer transplant and renal ischemia-reperfusion related questions, I have not thought it fruitful to persue the same in prostatitis.

In a recent exchange I had with Dr Theoharides, I asked him if the studies he is aiming to do will look not only at whether stress causes mast cell degranulation in murine urogenital tissues (which I believe has already been shown), but also *how* this occurs. Dr Jerome Weiss postulates in this article: http://www.jmweissmd.com/article.htm that stress/anxiety causes a primitive tensing or clenching reaction in the pelvis. So I'd like to know if the mice are tensing their pelvic muscles, and thereby causing neuropathy, and hence irritating mast cells.

Dr Theo responded that they will induce inflammatory cystitis, with or without stress, in a variety of genetically deficient animals in order to identify the neurohormones involved.

So it looks as though nobody will be monitoring the pelvic muscles in these rodents, and that's a pity.

And there is another important question. It is possible to breed a type of rodent ("genetically deficient") that will get an inflamed bladder pretty reliably, without having to expose it to stress (like confinement in a tiny box where it cannot move - yes, cruel, I know).

But WHY do these specially bred rodents get inflamed bladders, or spontaneous CPPS/PM? Is it only because they have a genetic weakness that makes them get it, no matter what? Or is it because they are very nervy, anxious rodents that experience high anxiety and stress just by being alive, tensing their tiny little mousy pelvic muscles as they go?

And lastly, they may have inflammation in their urogenital tracts, but are they experiencing pain? Is someone looking at their brain patterns to see if the pain centres are stimulated?

A lot of questions, and maybe $1M is not enough to answer them all ...