Neurological Basis of hypersenstivity?

Neurological Basis of hypersenstivity?

Hello,


Though it is not indicated, still I want to know that, can there be
some neurological basis of hypersentivities, allergy, autoimmunity
etc.? How an alergen contact with skin can trigger alergic response
without neurological basis? How hypersentivities can be persisitent
for whole life or prolonged time in consideration of cellular life
cycles other than of nerve cells?

Best wishes.

Re: Neurological Basis of hypersenstivity?

On Aug 28, 8:51 pm, Kumar <lordshiva5...@gmail . com > wrote:
> Hello,
>
> Though it is not indicated, still I want to know that, can there be
> some neurological basis of hypersentivities, allergy, autoimmunity
> etc.? How an alergen contact with skin can trigger alergic response
> without neurological basis? How hypersentivities can be persisitent
> for whole life or prolonged time in consideration of cellular life
> cycles other than of nerve cells?
>
> Best wishes.

No, there is no neurological basis, not that I knew of. The
hypersensitivity persists that long because the human body has memory-
B and memory-T-cells.

Re: Neurological Basis of hypersenstivity?

On Aug 29, 12:44 am, SanHolo <help.you.i....@gmail . com > wrote:
> On Aug 28, 8:51 pm, Kumar <lordshiva5...@gmail . com > wrote:
>
> > Hello,
>
> > Though it is not indicated, still I want to know that, can there be
> > some neurological basis of hypersentivities, allergy, autoimmunity
> > etc.? How an alergen contact with skin can trigger alergic response
> > without neurological basis? How hypersentivities can be persisitent
> > for whole life or prolonged time in consideration of cellular life
> > cycles other than of nerve cells?
>
> > Best wishes.
>
> No, there is no neurological basis, not that I knew of. The
> hypersensitivity persists that long because the human body has memory-
> B and memory-T-cells.

How a contact to skin can stimulate hypersentivity?

Re: Neurological Basis of hypersenstivity?

Dendritic cells, langerhans, B cells and T cells Mast cells(?).

* cmmg.biosci.wayne.edu/asg/dendritic.html

The neurological basis is an interesting question, not one I would dismiss
through lack of evidence but rather because no-one has really looked for
such evidence. You would need to look for studies on stress and
immunological function. Do not assume stress represses the immune response,
the initial elements (CRF, ACTH) can have activating elements (eg. CRF on
mast cells) long before glucocorticoids can reach sufficient levels to
suppress the response. Look up studies on allergies and depression, stuff
like that.

Mast cells are important players in allergies, they can degranulate
pro-inflammatory agents very quickly ... .

Incidentally, schizophrenics demonstrate altered immune responses.

Now stop asking interesting questions, I have better things to do than once
again get obsessed with neuroimmunology.



"Kumar" <lordshiva5753@gmail . com > wrote in message
news:1188366729.700904.151700@m37g2000prh.googlegroups . com ...
> On Aug 29, 12:44 am, SanHolo <help.you.i....@gmail . com > wrote:
> > On Aug 28, 8:51 pm, Kumar <lordshiva5...@gmail . com > wrote:
> >
> > > Hello,
> >
> > > Though it is not indicated, still I want to know that, can there be
> > > some neurological basis of hypersentivities, allergy, autoimmunity
> > > etc.? How an alergen contact with skin can trigger alergic response
> > > without neurological basis? How hypersentivities can be persisitent
> > > for whole life or prolonged time in consideration of cellular life
> > > cycles other than of nerve cells?
> >
> > > Best wishes.
> >
> > No, there is no neurological basis, not that I knew of. The
> > hypersensitivity persists that long because the human body has memory-
> > B and memory-T-cells.
>
> How a contact to skin can stimulate hypersentivity?
>

Re: Neurological Basis of hypersenstivity?

On Aug 29, 1:06 pm, "John H." <bingb...@goaway . com .au> wrote:
> Dendritic cells, langerhans, B cells and T cells Mast cells(?).
>
> * cmmg.biosci.wayne.edu/asg/dendritic.html
>
> The neurological basis is an interesting question, not one I would dismiss
> through lack of evidence but rather because no-one has really looked for
> such evidence. You would need to look for studies on stress and
> immunological function. Do not assume stress represses the immune response,
> the initial elements (CRF, ACTH) can have activating elements (eg. CRF on
> mast cells) long before glucocorticoids can reach sufficient levels to
> suppress the response. Look up studies on allergies and depression, stuff
> like that.
>
> Mast cells are important players in allergies, they can degranulate
> pro-inflammatory agents very quickly ... .
>
> Incidentally, schizophrenics demonstrate altered immune responses.
>
> Now stop asking interesting questions, I have better things to do than once
> again get obsessed with neuroimmunology.
>
> "Kumar" <lordshiva5...@gmail . com > wrote in message
>
> news:1188366729.700904.151700@m37g2000prh.googlegroups . com ...
>
>
>
> > On Aug 29, 12:44 am, SanHolo <help.you.i....@gmail . com > wrote:
> > > On Aug 28, 8:51 pm, Kumar <lordshiva5...@gmail . com > wrote:
>
> > > > Hello,
>
> > > > Though it is not indicated, still I want to know that, can there be
> > > > some neurological basis of hypersentivities, allergy, autoimmunity
> > > > etc.? How an alergen contact with skin can trigger alergic response
> > > > without neurological basis? How hypersentivities can be persisitent
> > > > for whole life or prolonged time in consideration of cellular life
> > > > cycles other than of nerve cells?
>
> > > > Best wishes.
>
> > > No, there is no neurological basis, not that I knew of. The
> > > hypersensitivity persists that long because the human body has memory-
> > > B and memory-T-cells.
>
> > How a contact to skin can stimulate hypersentivity?- Hide quoted text -
>
> - Show quoted text -

Thanks and sorry. I think, studying stress is the right choice. Stress
asthma, eczema due to mental involvements etc. are there.

Re: Neurological Basis of hypersenstivity?

On Aug 29, 1:10 pm, Kumar <lordshiva5...@gmail . com > wrote:
> On Aug 29, 1:06 pm, "John H." <bingb...@goaway . com .au> wrote:
>
>
"mast cell (or mastocyte) is a resident cell of several types of
tissues and contains many granules rich in histamine and heparin.
Although best known for their role in allergy and anaphylaxis, mast
cells play an important protective role as well, being intimately
involved in wound healing and defense against pathogens.....Histamine
dilates post capillary venules, activates the endothelium, and
increases blood vessel permeability. This leads to local edema
(swelling), warmth, redness, and the attraction of other inflammatory
cells to the site of release. **It also irritates nerve endings
(leading to itching or pain). ** * en.wikipedia.org/wiki/Mast_cell
"

How **** are related to this topic? What happens after irritation to
nerve endings resulting itching ans pain? Does it promote some other
physiological activities related to hypersensitivity forming a
neurological basis?

Re: Neurological Basis of hypersenstivity?

I told you not to ask ...

You'll need to start investigating how the immune system facilitates pain.
The best example of this is neuropathic pain, microglia being strongly
implicated here as these release pro-inflammatory mediators that can
increase pain levels. (This offers some insight into why CB2 agonists can
reduce neuropathic pain because microglia do express this receptor and
cannabinoids have shown some efficacy in treating neuropathic pain.) For
example, interleukin 1 can induce substance p release, the latter seems to
play some role in pain. What is "irritating" the nerves is immunological
agents. For example, some interleukins (forget which one) can sensitise
sensory nerves.

So look up "depression and pain" - depression is often marked by increased
expression of pro-inflammatory mediators and depressives, I think, are more
sensitive to pain.

Remember now, Interleukin 6! Can act as a pro-inflammatory stimulator.

PS: No need to apologise Kumar, in this realm everyone is in the woods!
Beautiful forest though.


Regards,


John.

"Kumar" <lordshiva5753@gmail . com > wrote in message
news:1188386782.182280.254000@l22g2000prc.googlegroups . com ...
> On Aug 29, 1:10 pm, Kumar <lordshiva5...@gmail . com > wrote:
> > On Aug 29, 1:06 pm, "John H." <bingb...@goaway . com .au> wrote:
> >
> >
> "mast cell (or mastocyte) is a resident cell of several types of
> tissues and contains many granules rich in histamine and heparin.
> Although best known for their role in allergy and anaphylaxis, mast
> cells play an important protective role as well, being intimately
> involved in wound healing and defense against pathogens.....Histamine
> dilates post capillary venules, activates the endothelium, and
> increases blood vessel permeability. This leads to local edema
> (swelling), warmth, redness, and the attraction of other inflammatory
> cells to the site of release. **It also irritates nerve endings
> (leading to itching or pain). ** * en.wikipedia.org/wiki/Mast_cell
> "
>
> How **** are related to this topic? What happens after irritation to
> nerve endings resulting itching ans pain? Does it promote some other
> physiological activities related to hypersensitivity forming a
> neurological basis?
>
>
>

Re: Neurological Basis of hypersenstivity?

On Aug 29, 7:47 pm, "John H." <bingb...@goaway . com .au> wrote:
> I told you not to ask ...
>
> You'll need to start investigating how the immune system facilitates pain.
> The best example of this is neuropathic pain, microglia being strongly
> implicated here as these release pro-inflammatory mediators that can
> increase pain levels. (This offers some insight into why CB2 agonists can
> reduce neuropathic pain because microglia do express this receptor and
> cannabinoids have shown some efficacy in treating neuropathic pain.) For
> example, interleukin 1 can induce substance p release, the latter seems to
> play some role in pain. What is "irritating" the nerves is immunological
> agents. For example, some interleukins (forget which one) can sensitise
> sensory nerves.
>
> So look up "depression and pain" - depression is often marked by increased
> expression of pro-inflammatory mediators and depressives, I think, are more
> sensitive to pain.
>
> Remember now, Interleukin 6! Can act as a pro-inflammatory stimulator.
>
> PS: No need to apologise Kumar, in this realm everyone is in the woods!
> Beautiful forest though.
>
> Regards,
>
> John.
>
> "Kumar" <lordshiva5...@gmail . com > wrote in message
>
> news:1188386782.182280.254000@l22g2000prc.googlegroups . com ...
>
>
>
> > On Aug 29, 1:10 pm, Kumar <lordshiva5...@gmail . com > wrote:
> > > On Aug 29, 1:06 pm, "John H." <bingb...@goaway . com .au> wrote:
>
> > "mast cell (or mastocyte) is a resident cell of several types of
> > tissues and contains many granules rich in histamine and heparin.
> > Although best known for their role in allergy and anaphylaxis, mast
> > cells play an important protective role as well, being intimately
> > involved in wound healing and defense against pathogens.....Histamine
> > dilates post capillary venules, activates the endothelium, and
> > increases blood vessel permeability. This leads to local edema
> > (swelling), warmth, redness, and the attraction of other inflammatory
> > cells to the site of release. **It also irritates nerve endings
> > (leading to itching or pain). ** * en.wikipedia.org/wiki/Mast_cell
> > "
>
> > How **** are related to this topic? What happens after irritation to
> > nerve endings resulting itching ans pain? Does it promote some other
> > physiological activities related to hypersensitivity forming a
> > neurological basis?- Hide quoted text -
>
> - Show quoted text -

Thanks good teaching, Btw, whether such pain is just patholgical or
also have some beneficial purpose for survival?

Re: Neurological Basis of hypersenstivity?


> Thanks good teaching, Btw, whether such pain is just patholgical or
> also have some beneficial purpose for survival?

Like many, perhaps all, biological processes, "pain" is what I call a
"probability hit". That is, strategies have emerged that in the main can
address the problem but there are significant exceptions. Consider this
Kumar: amongst the commonly prescribed drugs are anti-inflammatories. Many
pain killers target cox 2, a rate limiting enzyme for the production of some
inflammatory mediators.

Inflammation is a "danger signal" so it is not surprising that inflammation
induces pain because pain prevents us from further damage to the area. If
you are clinging to the "self nonself" model of immunology throw it out and
trample it down. It's dead. Look up Poly Matzinger "danger theory". That
earlier link I gave you, towards the middle of that page, is a link to a
very short but clear essay by Polly on this issue. This is now the accepted
model in immunology and it will help you understand the immune system. You
should also look at Janeway's ideas of PAMPs.


"Kumar" <lordshiva5753@gmail . com > wrote in message
news:1188444317.421297.24100@q5g2000prf.googlegroups . com ...
> On Aug 29, 7:47 pm, "John H." <bingb...@goaway . com .au> wrote:
> > I told you not to ask ...
> >
> > You'll need to start investigating how the immune system facilitates
pain.
> > The best example of this is neuropathic pain, microglia being strongly
> > implicated here as these release pro-inflammatory mediators that can
> > increase pain levels. (This offers some insight into why CB2 agonists
can
> > reduce neuropathic pain because microglia do express this receptor and
> > cannabinoids have shown some efficacy in treating neuropathic pain.) For
> > example, interleukin 1 can induce substance p release, the latter seems
to
> > play some role in pain. What is "irritating" the nerves is immunological
> > agents. For example, some interleukins (forget which one) can sensitise
> > sensory nerves.
> >
> > So look up "depression and pain" - depression is often marked by
increased
> > expression of pro-inflammatory mediators and depressives, I think, are
more
> > sensitive to pain.
> >
> > Remember now, Interleukin 6! Can act as a pro-inflammatory stimulator.
> >
> > PS: No need to apologise Kumar, in this realm everyone is in the woods!
> > Beautiful forest though.
> >
> > Regards,
> >
> > John.
> >
> > "Kumar" <lordshiva5...@gmail . com > wrote in message
> >
> > news:1188386782.182280.254000@l22g2000prc.googlegroups . com ...
> >
> >
> >
> > > On Aug 29, 1:10 pm, Kumar <lordshiva5...@gmail . com > wrote:
> > > > On Aug 29, 1:06 pm, "John H." <bingb...@goaway . com .au> wrote:
> >
> > > "mast cell (or mastocyte) is a resident cell of several types of
> > > tissues and contains many granules rich in histamine and heparin.
> > > Although best known for their role in allergy and anaphylaxis, mast
> > > cells play an important protective role as well, being intimately
> > > involved in wound healing and defense against pathogens.....Histamine
> > > dilates post capillary venules, activates the endothelium, and
> > > increases blood vessel permeability. This leads to local edema
> > > (swelling), warmth, redness, and the attraction of other inflammatory
> > > cells to the site of release. **It also irritates nerve endings
> > > (leading to itching or pain). ** * en.wikipedia.org/wiki/Mast_cell
> > > "
> >
> > > How **** are related to this topic? What happens after irritation to
> > > nerve endings resulting itching ans pain? Does it promote some other
> > > physiological activities related to hypersensitivity forming a
> > > neurological basis?- Hide quoted text -
> >
> > - Show quoted text -
>>

Re: Neurological Basis of hypersenstivity?

Apart from what you have taught, can localized pain be meant to
concentrate nervous system's promoted concentration of physiological
activities at the point of pain? Pain may tell a problem at any point.
So the cocenration of physiological activities may be needed to take
care of that problem at that point. When I pinch or pin or scratch a
point on my hand, I do feel somewhat concentrating at that point. Best
regards.

On Aug 30, 12:24 pm, "John H." <bingb...@goaway . com .au> wrote:
> > Thanks good teaching, Btw, whether such pain is just patholgical or
> > also have some beneficial purpose for survival?
>
> Like many, perhaps all, biological processes, "pain" is what I call a
> "probability hit". That is, strategies have emerged that in the main can
> address the problem but there are significant exceptions. Consider this
> Kumar: amongst the commonly prescribed drugs are anti-inflammatories. Many
> pain killers target cox 2, a rate limiting enzyme for the production of some
> inflammatory mediators.
>
> Inflammation is a "danger signal" so it is not surprising that inflammation
> induces pain because pain prevents us from further damage to the area. If
> you are clinging to the "self nonself" model of immunology throw it out and
> trample it down. It's dead. Look up Poly Matzinger "danger theory". That
> earlier link I gave you, towards the middle of that page, is a link to a
> very short but clear essay by Polly on this issue. This is now the accepted
> model in immunology and it will help you understand the immune system. You
> should also look at Janeway's ideas of PAMPs.
>
> "Kumar" <lordshiva5...@gmail . com > wrote in message
>
> news:1188444317.421297.24100@q5g2000prf.googlegroups . com ...
>
>
>
> > On Aug 29, 7:47 pm, "John H." <bingb...@goaway . com .au> wrote:
> > > I told you not to ask ...
>
> > > You'll need to start investigating how the immune system facilitates
> pain.
> > > The best example of this is neuropathic pain, microglia being strongly
> > > implicated here as these release pro-inflammatory mediators that can
> > > increase pain levels. (This offers some insight into why CB2 agonists
> can
> > > reduce neuropathic pain because microglia do express this receptor and
> > > cannabinoids have shown some efficacy in treating neuropathic pain.) For
> > > example, interleukin 1 can induce substance p release, the latter seems
> to
> > > play some role in pain. What is "irritating" the nerves is immunological
> > > agents. For example, some interleukins (forget which one) can sensitise
> > > sensory nerves.
>
> > > So look up "depression and pain" - depression is often marked by
> increased
> > > expression of pro-inflammatory mediators and depressives, I think, are
> more
> > > sensitive to pain.
>
> > > Remember now, Interleukin 6! Can act as a pro-inflammatory stimulator.
>
> > > PS: No need to apologise Kumar, in this realm everyone is in the woods!
> > > Beautiful forest though.
>
> > > Regards,
>
> > > John.
>
> > > "Kumar" <lordshiva5...@gmail . com > wrote in message
>
> > >news:1188386782.182280.254000@l22g2000prc.googlegroups . com ...
>
> > > > On Aug 29, 1:10 pm, Kumar <lordshiva5...@gmail . com > wrote:
> > > > > On Aug 29, 1:06 pm, "John H." <bingb...@goaway . com .au> wrote:
>
> > > > "mast cell (or mastocyte) is a resident cell of several types of
> > > > tissues and contains many granules rich in histamine and heparin.
> > > > Although best known for their role in allergy and anaphylaxis, mast
> > > > cells play an important protective role as well, being intimately
> > > > involved in wound healing and defense against pathogens.....Histamine
> > > > dilates post capillary venules, activates the endothelium, and
> > > > increases blood vessel permeability. This leads to local edema
> > > > (swelling), warmth, redness, and the attraction of other inflammatory
> > > > cells to the site of release. **It also irritates nerve endings
> > > > (leading to itching or pain). ** * en.wikipedia.org/wiki/Mast_cell
> > > > "
>
> > > > How **** are related to this topic? What happens after irritation to
> > > > nerve endings resulting itching ans pain? Does it promote some other
> > > > physiological activities related to hypersensitivity forming a
> > > > neurological basis?- Hide quoted text -
>
> > > - Show quoted text -- Hide quoted text -
>
> - Show quoted text -

Re: Neurological Basis of hypersenstivity?

Now you're heading into territory I'm not familiar with. I don't really
study this stuff anymore so read on at your own peril.



Simple principles of reinforcement offer insight. An ongoing signal
basically makes it more likely that even weak initiators will keep it going.
This can happen at many levels, DRG neurons (spinal cord) seem important in
this regard. It wouldn't surprise me if in the brain there are also
alterations that facilitate the ongoing signal transmission.

This may offer some insight into why learning to ignore pain can have its
benefits. It is amazing how when concentrated one can become oblivious to
pain. A recent study claimed that a "macho attitude" can be preventive
against PTSD. That goes against conventional wisdom but has support from
other studies indicating that making people rehearse traumatic events can
make matters worse. This was always common sense to me. Again, simple ideas
about reinforcement, while not offering a full explanation, can offer
insights into how these processes evolve.

And to contradict myself, there are some fascinating hints suggesting that
the relative levels of activation in the frontal cortices correlates with
the basic "balance" of the immune response. Increased left side activity
tends to move the immune response into a "Th 2" type response, while the
right a Th 1. What is fascinating about this is that in depression there can
be an imbalance in these levels of activity. Happiness is also associated
with a stronger left side activity and a better immune response. Very
tentative stuff here Kumar.

Back to the periphery.

The other level is at the periphery. This is where the immunological
component can become very important, though I would exclude the possiblity
of this being important at the DRG level. The neurons basically are in an
environment that facilitates signal transmission. Often an inflammatory
environment. This remains one of the great challenges in immunology:
controlling inflammation. There are even studies showing direct correlations
between age related cognitive impairment and the expression of inflammatory
mediators (il1,tnf, il6, haptoglobin also implicated). Pollmacher has done
studies showing that even very small doses of LPS can induce cognitive
deficits.


A key player in the ongoing inflammation could well be dendritic cells. I
have read studies showing that long after cessation of cerebral inflammation
DCs remain present in the relevant region(the big unanswered question here
is whether these DCs are of external origin or from microglia undergoing
transformation via GM-CSF). This has very important implicatoins for
inflammation because DCs express il-12 which is a strong driver of the same.
At the clinical level there is evidence to suggest that injury can leave an
area "immunologically sensitised" and I suspect it is the ongoing presence
of DCs that are playing an important role here. And I just may be onto
something because:

Nat Med 1999 Nov;5(11):1249-Natural adjuvants: endogenous activators of
dendritic cells.


Gallucci S, Lolkema M, Matzinger P.


Ghost Lab, T cell Tolerance and Memory Section, Laboratory for Cellular and
Molecular Immunology, National Institutes of Allergy and Infectious
Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA.
sgallucci@niaid.nih.gov


Dendritic cells, the most potent antigen-presenting cells, need to be
activated before they can function to initiate an immune response. We report
here that, in the absence of any foreign substances, dendritic cells can be
activated by endogenous signals received from cells that are stressed,
virally infected or killed necrotically, but not by healthy cells or those
dying apoptotically. Injected in vivo with an antigen, the endogenous
activating substances can function as natural adjuvants to stimulate a
primary immune response, and they may represent the natural initiators of
transplant rejection, spontaneous tumor rejection, and some forms of
autoimmunity.


PMID: 10545990 [PubMed - indexed for MEDLINE]



So the "concentration" you are looking for is probably at the periphery.
That will not only include the immunological component but also the nerves
may undergo morphological changes that facilitate increased transmission.

This is a vast area Kumar, I've tried to give you a glimpse. I really need
to get back to some reading .... .

Hope this helps,



John.




"Kumar" <lordshiva5753@gmail . com > wrote in message
news:1188463753.394085.141700@x40g2000prg.googlegroups . com ...
> Apart from what you have taught, can localized pain be meant to
> concentrate nervous system's promoted concentration of physiological
> activities at the point of pain? Pain may tell a problem at any point.
> So the cocenration of physiological activities may be needed to take
> care of that problem at that point. When I pinch or pin or scratch a
> point on my hand, I do feel somewhat concentrating at that point. Best
> regards.
>
> On Aug 30, 12:24 pm, "John H." <bingb...@goaway . com .au> wrote:
> > > Thanks good teaching, Btw, whether such pain is just patholgical or
> > > also have some beneficial purpose for survival?
> >
> > Like many, perhaps all, biological processes, "pain" is what I call a
> > "probability hit". That is, strategies have emerged that in the main can
> > address the problem but there are significant exceptions. Consider this
> > Kumar: amongst the commonly prescribed drugs are anti-inflammatories.
Many
> > pain killers target cox 2, a rate limiting enzyme for the production of
some
> > inflammatory mediators.
> >
> > Inflammation is a "danger signal" so it is not surprising that
inflammation
> > induces pain because pain prevents us from further damage to the area.
If
> > you are clinging to the "self nonself" model of immunology throw it out
and
> > trample it down. It's dead. Look up Poly Matzinger "danger theory". That
> > earlier link I gave you, towards the middle of that page, is a link to a
> > very short but clear essay by Polly on this issue. This is now the
accepted
> > model in immunology and it will help you understand the immune system.
You
> > should also look at Janeway's ideas of PAMPs.
> >
> > "Kumar" <lordshiva5...@gmail . com > wrote in message
> >
> > news:1188444317.421297.24100@q5g2000prf.googlegroups . com ...
> >
> >
> >
> > > On Aug 29, 7:47 pm, "John H." <bingb...@goaway . com .au> wrote:
> > > > I told you not to ask ...
> >
> > > > You'll need to start investigating how the immune system facilitates
> > pain.
> > > > The best example of this is neuropathic pain, microglia being
strongly
> > > > implicated here as these release pro-inflammatory mediators that can
> > > > increase pain levels. (This offers some insight into why CB2
agonists
> > can
> > > > reduce neuropathic pain because microglia do express this receptor
and
> > > > cannabinoids have shown some efficacy in treating neuropathic pain.)
For
> > > > example, interleukin 1 can induce substance p release, the latter
seems
> > to
> > > > play some role in pain. What is "irritating" the nerves is
immunological
> > > > agents. For example, some interleukins (forget which one) can
sensitise
> > > > sensory nerves.
> >
> > > > So look up "depression and pain" - depression is often marked by
> > increased
> > > > expression of pro-inflammatory mediators and depressives, I think,
are
> > more
> > > > sensitive to pain.
> >
> > > > Remember now, Interleukin 6! Can act as a pro-inflammatory
stimulator.
> >
> > > > PS: No need to apologise Kumar, in this realm everyone is in the
woods!
> > > > Beautiful forest though.
> >
> > > > Regards,
> >
> > > > John.
> >
> > > > "Kumar" <lordshiva5...@gmail . com > wrote in message
> >
> > > >news:1188386782.182280.254000@l22g2000prc.googlegroups . com ...
> >
> > > > > On Aug 29, 1:10 pm, Kumar <lordshiva5...@gmail . com > wrote:
> > > > > > On Aug 29, 1:06 pm, "John H." <bingb...@goaway . com .au> wrote:
> >
> > > > > "mast cell (or mastocyte) is a resident cell of several types of
> > > > > tissues and contains many granules rich in histamine and heparin.
> > > > > Although best known for their role in allergy and anaphylaxis,
mast
> > > > > cells play an important protective role as well, being intimately
> > > > > involved in wound healing and defense against
pathogens.....Histamine
> > > > > dilates post capillary venules, activates the endothelium, and
> > > > > increases blood vessel permeability. This leads to local edema
> > > > > (swelling), warmth, redness, and the attraction of other
inflammatory
> > > > > cells to the site of release. **It also irritates nerve endings
> > > > > (leading to itching or pain).
** * en.wikipedia.org/wiki/Mast_cell
> > > > > "
> >
> > > > > How **** are related to this topic? What happens after irritation
to
> > > > > nerve endings resulting itching ans pain? Does it promote some
other
> > > > > physiological activities related to hypersensitivity forming a
> > > > > neurological basis?- Hide quoted text -
> >
> > > > - Show quoted text -- Hide quoted text -
> >
> > - Show quoted text -
>
>

Re: Neurological Basis of hypersenstivity?

Thanks again. Yes your teaching is helping me.

I read about recent research that there is a physical basis of reward
expectation, placebo etc. i.e. dopamine release in brain. As such
there can also be a physical basis of punisment, pain or all
sensations and emotions somewhat cephalic phase effect by sensing any
food. There is an obslete rule (re-thought as hormesis);

"Arndt's l. , Arndt-Schulz l. weak stimuli increase physiologic
activity, moderate stimuli inhibit activity, and very strong stimuli
abolish activity. See also hormesis.
hormesis (hor=B7me=B7sis) (hor-me=B4sis) [Gr. horm sis rapid motion] the
stimulating or beneficial effect of small doses of a toxic substance
that at higher doses has an inhibitory or adverse effect." from
Dorlands medical dict. "

I think, above can be relevant to physiological activities either by
immune response and via neurological involvement. In homeopathy, they
said to give an exteremely diluted dose of any hetrogenous or
homogenous substance. This probably may be working on hetrogenous or
odd exposure of very low dose stimulating neurological route.

In all such, consideration, neurolgical basis of pain due to
irritation and hypersenstivities can be possible, benefitting by
either removing from the cause and by encouraging/concentrating
neurological mediated physiological activities for increasing or
continuing immune responses and to remain away from other mechanical
sressors. Easyness/pleasure/reward/enjoyment AND uneasyness/punishment/
dyspleasure/pain etc. can be opposing sensations which may be having
physical basis in brain resuting physiological basis in body and
effect accordingly. Is it ok?

Sorry, If I bothered you much or deviated, in this post, thought I
think, I am not clear.




On Aug 30, 5:55 pm, "John H." <bingb...@goaway . com .au> wrote:
> Now you're heading into territory I'm not familiar with. I don't really
> study this stuff anymore so read on at your own peril.
>
> Simple principles of reinforcement offer insight. An ongoing signal
> basically makes it more likely that even weak initiators will keep it goi=
ng.
> This can happen at many levels, DRG neurons (spinal cord) seem important =
in
> this regard. It wouldn't surprise me if in the brain there are also
> alterations that facilitate the ongoing signal transmission.
>
> This may offer some insight into why learning to ignore pain can have its
> benefits. It is amazing how when concentrated one can become oblivious to
> pain. A recent study claimed that a "macho attitude" can be preventive
> against PTSD. That goes against conventional wisdom but has support from
> other studies indicating that making people rehearse traumatic events can
> make matters worse. This was always common sense to me. Again, simple ide=
as
> about reinforcement, while not offering a full explanation, can offer
> insights into how these processes evolve.
>
> And to contradict myself, there are some fascinating hints suggesting that
> the relative levels of activation in the frontal cortices correlates with
> the basic "balance" of the immune response. Increased left side activity
> tends to move the immune response into a "Th 2" type response, while the
> right a Th 1. What is fascinating about this is that in depression there =
can
> be an imbalance in these levels of activity. Happiness is also associated
> with a stronger left side activity and a better immune response. Very
> tentative stuff here Kumar.
>
> Back to the periphery.
>
> The other level is at the periphery. This is where the immunological
> component can become very important, though I would exclude the possiblity
> of this being important at the DRG level. The neurons basically are in an
> environment that facilitates signal transmission. Often an inflammatory
> environment. This remains one of the great challenges in immunology:
> controlling inflammation. There are even studies showing direct correlati=
ons
> between age related cognitive impairment and the expression of inflammato=
ry
> mediators (il1,tnf, il6, haptoglobin also implicated). Pollmacher has done
> studies showing that even very small doses of LPS can induce cognitive
> deficits.
>
> A key player in the ongoing inflammation could well be dendritic cells. I
> have read studies showing that long after cessation of cerebral inflammat=
ion
> DCs remain present in the relevant region(the big unanswered question here
> is whether these DCs are of external origin or from microglia undergoing
> transformation via GM-CSF). This has very important implicatoins for
> inflammation because DCs express il-12 which is a strong driver of the sa=
me.
> At the clinical level there is evidence to suggest that injury can leave =
an
> area "immunologically sensitised" and I suspect it is the ongoing presence
> of DCs that are playing an important role here. And I just may be onto
> something because:
>
> Nat Med 1999 Nov;5(11):1249-Natural adjuvants: endogenous activators of
> dendritic cells.
>
> Gallucci S, Lolkema M, Matzinger P.
>
> Ghost Lab, T cell Tolerance and Memory Section, Laboratory for Cellular a=
nd
> Molecular Immunology, National Institutes of Allergy and Infectious
> Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA.
> sgallu...@niaid.nih.gov
>
> Dendritic cells, the most potent antigen-presenting cells, need to be
> activated before they can function to initiate an immune response. We rep=
ort
> here that, in the absence of any foreign substances, dendritic cells can =
be
> activated by endogenous signals received from cells that are stressed,
> virally infected or killed necrotically, but not by healthy cells or those
> dying apoptotically. Injected in vivo with an antigen, the endogenous
> activating substances can function as natural adjuvants to stimulate a
> primary immune response, and they may represent the natural initiators of
> transplant rejection, spontaneous tumor rejection, and some forms of
> autoimmunity.
>
> PMID: 10545990 [PubMed - indexed for MEDLINE]
>
> So the "concentration" you are looking for is probably at the periphery.
> That will not only include the immunological component but also the nerves
> may undergo morphological changes that facilitate increased transmission.
>
> This is a vast area Kumar, I've tried to give you a glimpse. I really need
> to get back to some reading .... .
>
> Hope this helps,
>
> John.
>
> "Kumar" <lordshiva5...@gmail . com > wrote in message
>
> news:1188463753.394085.141700@x40g2000prg.googlegroups . com ...
>
>
>
> > Apart from what you have taught, can localized pain be meant to
> > concentrate nervous system's promoted concentration of physiological
> > activities at the point of pain? Pain may tell a problem at any point.
> > So the cocenration of physiological activities may be needed to take
> > care of that problem at that point. When I pinch or pin or scratch a
> > point on my hand, I do feel somewhat concentrating at that point. Best
> > regards.
>
> > On Aug 30, 12:24 pm, "John H." <bingb...@goaway . com .au> wrote:
> > > > Thanks good teaching, Btw, whether such pain is just patholgical or
> > > > also have some beneficial purpose for survival?
>
> > > Like many, perhaps all, biological processes, "pain" is what I call a
> > > "probability hit". That is, strategies have emerged that in the main =
can
> > > address the problem but there are significant exceptions. Consider th=
is
> > > Kumar: amongst the commonly prescribed drugs are anti-inflammatories.
> Many
> > > pain killers target cox 2, a rate limiting enzyme for the production =
of
> some
> > > inflammatory mediators.
>
> > > Inflammation is a "danger signal" so it is not surprising that
> inflammation
> > > induces pain because pain prevents us from further damage to the area.
> If
> > > you are clinging to the "self nonself" model of immunology throw it o=
ut
> and
> > > trample it down. It's dead. Look up Poly Matzinger "danger theory". T=
hat
> > > earlier link I gave you, towards the middle of that page, is a link t=
o a
> > > very short but clear essay by Polly on this issue. This is now the
> accepted
> > > model in immunology and it will help you understand the immune system.
> You
> > > should also look at Janeway's ideas of PAMPs.
>
> > > "Kumar" <lordshiva5...@gmail . com > wrote in message
>
> > >news:1188444317.421297.24100@q5g2000prf.googlegroups . com ...
>
> > > > On Aug 29, 7:47 pm, "John H." <bingb...@goaway . com .au> wrote:
> > > > > I told you not to ask ...
>
> > > > > You'll need to start investigating how the immune system facilita=
tes
> > > pain.
> > > > > The best example of this is neuropathic pain, microglia being
> strongly
> > > > > implicated here as these release pro-inflammatory mediators that =
can
> > > > > increase pain levels. (This offers some insight into why CB2
> agonists
> > > can
> > > > > reduce neuropathic pain because microglia do express this receptor
> and
> > > > > cannabinoids have shown some efficacy in treating neuropathic pai=
n=2E)
> For
> > > > > example, interleukin 1 can induce substance p release, the latter
> seems
> > > to
> > > > > play some role in pain. What is "irritating" the nerves is
> immunological
> > > > > agents. For example, some interleukins (forget which one) can
> sensitise
> > > > > sensory nerves.
>
> > > > > So look up "depression and pain" - depression is often marked by
> > > increased
> > > > > expression of pro-inflammatory mediators and depressives, I think,
> are
> > > more
> > > > > sensitive to pain.
>
> > > > > Remember now, Interleukin 6! Can act as a pro-inflammatory
> stimulator.
>
> > > > > PS: No need to apologise Kumar, in this realm everyone is in the
> woods!
> > > > > Beautiful forest though.
>
> > > > > Regards,
>
> > > > > John.
>
> > > > > "Kumar" <lordshiva5...@gmail . com > wrote in message
>
> > > > >news:1188386782.182280.254000@l22g2000prc.googlegroups . com ...
>
> > > > > > On Aug 29, 1:10 pm, Kumar <lordshiva5...@gmail . com > wrote:
> > > > > > > On Aug 29, 1:06 pm, "John H." <bingb...@goaway . com .au> wrote:
>
> > > > > > "mast cell (or mastocyte) is a resident cell of several types of
> > > > > > tissues and contains many granules rich in histamine and hepari=
n=2E
> > > > > > Although best known for their role in allergy and anaphylaxis,
> mast
> > > > > > cells play an important protective role as well, being intimate=
ly
> > > > > > involved in wound healing and defense against
>
> pathogens.....Histamine> > > > > dilates post capillary venules, activate=
s the endothelium, and
> > > > > > increases blood vessel permeability. This leads to local edema
> > > > > > (swelling), warmth, redness, and the attraction of other
> inflammatory
> > > > > > cells to the site of release. **It also irritates nerve endings
> > > > > > (leading to itching or pain).
>
> ** * en.wikipedia.org/wiki/Mast_cell
>
>
>
> > > > > > "
>
> > > > > > How **** are related to this topic? What happens after irritati=
on
> to
> > > > > > nerve endings resulting itching ans pain? Does it promote some
> other
> > > > > > physiological activities related to hypersensitivity forming a
> > > > > > neurological basis?- Hide quoted text -
>
> > > > > - Show quoted text -- Hide quoted text -
>
> > > - Show quoted text -- Hide quoted text -
>
> - Show quoted text -- Hide quoted text -
>
> - Show quoted text -