peripheral nerve damage during inflammation

Dr paul Mapp p.mapp at
Tue Mar 7 06:57:09 EST 1995

In article <3jdt14$jfp at>, dfb at says...
>In article <3j4ieo$hph at>,
>Dr paul Mapp <p.mapp at> wrote:
>>If anybody has any information regarding the existence or otherwise of 
>>data relating to the damage to periheral nerves by inflasmmatory 
>>responses I would be most interested to hear about it. Our own research 
>>appears to show that unmyelinated C fibres are particularly sensitive 
>>damage leading to a possible dysregulation of the maintenace of 
>>tone. Comments? Questions?
>There is one or more studies by J. Sato et al. who have shown that
>inflammation produces a newly acquired adrenergic sensitivity in 
>They presented posters about this at the last two Neuroscience meetings
>but I am not sure wherther it was published.
>This new adrenergic sensitivity is probably due to an upregulation of
>cathecolaminergic alpha2 receptors as it has been demontrated after
>peripheral nerve injury.
>The dysregulation of the vasculature you have mentioned has been also
>documented after partial peripheral injury and may be due to a decreased
>sympathetic input to the region (sympathetic nerves travel with
>sensory-motor nerves and are affected by the same injury). 
>I have not yet seen evidence for vasculature problem as a consequence of
>C-fiber dammage. What is your basis to think in that direction?
>Daniel Bossut
>dfb at
We have evidence that in rheumatoid arthritis (RA) there is damage to 
peripheral nerve fibres, both sensory and sympathetic (mapp etal 1993 
Neuroscience 37:143-153. Similarly in animal models of arthritis 
articular nerves are also damaged (Mapp et al 1994 Ann Rheum Dis 53: 
240-246) Since the joint is measuably hypoxic,hypercapnic and acidotic we 
believe that normal vasoregulation is disturbed but are unsure which is 
the primary mechanism. Since C fibres apparently release Substance P in 
normal healthy animals it might be thought that this contributes to 
normal vasomotor tone via the interaction of SP with endothelial cells 
and the subsequent release of that old favorite nitric oxide. Thus 
damaged C fibres could lead to unopposed vaso constriction. Thoughts?  

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