chilis

Curt Ashendel ashendel at aclcb.purdue.edu
Wed Nov 9 09:18:51 EST 1994


On Wed, 09 Nov 1994 12:59:34 +0400, 
David S. Huen  <smh1008 at cus.cam.ac.uk> wrote:

>In article <39p6so$3co at steele.ohsu.edu>, nishir at ohsu.edu (Rae Nishi) wrote:
>> Hope you can stand one more comment on this topic.  There are specific
>> receptors for capasicin on sensory neurons and they appear to be on the
>> ones that contain substance P and sense slow pain.  Application of
>> capsaicin causes depolarization of the sensory neuron by opening a
>> channels in the membrane.  Eating lots of capsaicin destroys the fibers
>> (probably by an excitotoxic mechanism).  That's why those who eat alot
>> of chillies are less sensitive to the pain.  In newborn rats injection
>> of capscaicin causes death of these sensory neurons. 
>
>I might well be mistaken but I thought that capsaicin activated the same
>class of protein kinase Cs as resiniferatoxin (a phorbol ester) ?
>
This is REALLY getting off the subject, but if I remember correctly, 
Resiniferatoxin (which technically is not a phorbol ester, but is 
structurally related to them) does not act on PKC, but is highly 
inflammatory to mouse skin.  I think Pete Blumberg at NIH found that it 
acts as a hihgly potent agonist for the capscaicin receptor.  

I also heard that birds do not have receptors for capscaicin and that if 
you put it on bird seed it keeps the squirrels from eating it, but has no 
affect on the birds. A guy I know patented this.  Isn't it odd how research 
on signaling and cancer leads to an "improved" bird food?


Curt Ashendel
Purdue University
West Lafayette, IN
ashendel at aclcb.purdue.edu



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