webslave a post of yours revisited

[scoobysnacks]

I'm sorry for all the posts lately, but I refuse to give up with this.

You once said this, and I think it gives me a pretty good understanding. Have you ever found an article or diagram like you speak of to explain it further???

"That's pretty impressive! It looks more and more as if the symptoms of CP/CPPS/IC are the result of a complex interplay between mind, muscles, nerves and immune system. Some trigger (injury, overtensed muscles due to stress, infection, allergy etc) sets up a persistent neural feedbak loop with windup, resulting in neuropeptides that stimulate the local immune system (mast cells) into a whole cascade of harmful chemicals affecting bladder, prostate and/or testicles.

If I had the time I'd do a diagram to illustrate this, buit I'm sure some enterprising researching urologist is already busy with it!"

What are neuropeptides and can I block them or inhibit them somehow???

Also care to elaborate or point to an article

thanks,

SS

[webslave]

The neuropeptides I refer to are the hormones created by the overstimulated nerves at their endings. An overstimulated or damaged nerve can do this weird thing. For instance, in experiments they have found that when using the rat model, injuring the central nervous system of the rat led to inflammation in the bladder (doesn't look like they checked the prostate). Appropriate controls were done to rule out viral infection as the direct cause and show that it was carried by the nerves.

J Neurosci 1998 Dec 1;18(23):10016-29

Activation of CNS circuits producing a neurogenic cystitis: evidence for centrally induced peripheral inflammation.

Jasmin L, Janni G, Manz HJ, Rabkin SD
Department of Neurosurgery, Georgetown University Medical Center, Washington, DC 20007, USA.

We present a model of neurogenic cystitis induced by viral infection of specific neuronal circuits of the rat CNS. Retrograde infection by pseudorabies virus (PRV) of neuronal populations neighboring those that innervate the bladder consistently led to a localized immune response in the CNS and bladder inflammation. Infection of bladder circuits themselves or of circuits distant from these rarely produced cystitis. Absence of virus in bladder and urine ruled out an infectious cystitis. Total denervation of the bladder, selective C-fiber deafferentation, or bladder sympathectomy prevented cystitis without affecting the CNS disease, indicating a neurogenic component to the inflammation. The integrity of central bladder-related circuits is necessary for the appearance of bladder inflammation, because only CNS lesions affecting bladder circuits, i.e., bilateral dorsolateral or ventrolateral funiculectomy, as well as bilateral lesions of Barrington's nucleus/locus coeruleus area, prevented bladder inflammation. The close proximity in the CNS of noninfected visceral circuits to infected somatic neurons would thus permit a bystander effect, leading to activation of the sensory and autonomic circuits innervating the bladder and resulting in a neurogenic inflammation localized to the bladder. The present study indicates that CNS dysfunction can bring about a peripheral inflammation.

The blocking or inhibiting of this pathway is the subject of research, but anyhting that lessens the tendency of mast cells to degranulate (Quercetin, ProstaProtek), or lessens the effects of the degranulation products (Quercetin, ProstaProtek, antihistamines, EsterC etc), will lessen symptoms.

[scoobysnacks]

Thank you