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Home > Archive > Herpes support > October 2006 > Topical Hot peppers and Calcium chewable.
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Topical Hot peppers and Calcium chewable.
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| Perl Molson 2006-10-12, 8:29 am |
| Here are 2 articles about hot peppers (capsaicin) and Ca:
we can corelate these 2 and the result may be surprising; are you
ready for a try out? (if you have a cold sore, open a red hot chilli
pepper
wipe it on the sore, then suck-up a Calcium chewable pill.
1)
http://www.jneurosci.org/cgi/conten...e211b7ce17#SEC2
Summary
The results presented in this paper contribute to understanding how
calcium feeds back to desensitize capsaicin-activated channels. The
importance of calcium in the desensitization of capsaicin responses is
not surprising considering the role of calcium in the desensitization
of other receptors, including the NMDA class of the glutamate receptor
family (Clark et al., 1990; Legendre et al., 1993) and the nicotinic
acetylcholine receptor (Scubon-Mulieri and Parsons, 1977). The
characterization of desensitization processes, such as those regulating
the capsaicin response in rat DRG neurons, is crucial to understanding
how sensory neurons can adapt their responses to repetitive stimuli in
their environment. Furthermore, the future development and
characterization of capsaicin analogs designed to combine increased
desensitizing properties with decreased pungency may lead to a more
effective therapeutic intervention for chronic pain conditions.
2)
http://vir.sgmjournals.org/cgi/content/full/84/5/1071
Capsaicin-induced reactivation of latent herpes simplex virus type 1 in
sensory neurons in culture
The desensitization of VR-1 at higher concentrations of capsaicin
suggests a protective mechanism of the neuron to shut off damaging Ca2+
influxes. Other investigators have noted desensitization of VR-1
following repeated stimulation with capsaicin in electrophysiology
experiments (Docherty et al., 1996; Koplas et al., 1997; Piper et al.,
1999). In these experiments, repeated exposure to capsaicin decreased
and eventually abolished calcium currents. Furthermore, other studies
have noted a decrease in mRNA levels of VR-1 following capsaicin
treatment, suggesting down-regulation of the receptor (Mezey et al.,
2000). The mechanism underlying this desensitization is unknown,
although it has been suggested that capsaicin desensitization may be
similar to calcium-dependent inactivation of the N-methyl D-aspartate
receptor (Docherty et al., 1996). This assumes that a particular
threshold of intracellular Ca2+ levels negatively affects channel
activity and gating (Koplas et al., 1997). Because capsaicin treatment
results in rapid VR-1 desensitization in electrophysiology experiments
and long-term desensitization in animal models, there may be two
components of this desensitization. One component may be attributed to
multiple ligand binding domains within particular regions on the
receptor that change the kinetics and gating properties of the channel.
The second component may involve receptor turnover. These two
components may regulate the internal calcium levels to ensure survival
of the neuron.
The neuron relies on calcium channels and non-selective ion channels
such as VR-1 to regulate intracellular calcium. Hence, VR-1 is found
not only at the nerve terminal, but throughout the axon and soma (Guo
et al., 1999). Additionally, the neuron expresses calcium-binding
proteins capable of chelating excess toxic levels of calcium,
preventing continuous stimulation and allowing cellular recovery
(Berridge, 1998). Prolonged Ca2+ increases due to a high-intensity
stimulus, such as a pain stimulus, causes hyperexcitation of the
neuron. This high-intensity stimulus causes a prolonged increase in
intracellular Ca2+, creating a wave of calcium that eventually reaches
the soma or cell body of the neuron (Usachev & Thayer, 1999). In the in
vitro model, this hyperexcitation may occur rapidly due to the fact
that we are stimulating not only the nerve terminal but also the cell
body. When hyperexcitation of a neuron occurs, these unusually elevated
intracellular calcium levels in the soma transition the transcriptional
machinery from a normal basal level to a highly active level (Buonanno
& Fields, 1999; West et al., 2001). Perhaps in response to this
increase in transcriptional activity in the neuron due to prolonged
Ca2+ stimulation, HSV-1 is able to induce the transcription of
immediate-early genes and begin a lytic infection. This may occur
either via a direct role through Ca2+-dependent transcription factors
or through an indirect activation of host-cell gene transcriptional
machinery that serendipitously initiates HSV-1 transcription.
| |
|
| Hmmm! I think if I put a hot peppr on a cold sore I might like the new sky
light I would create!
Wanda : )
"Perl Molson" <beatadje@email.com> wrote in message
news:1160640101.161340.114270@i3g2000cwc.googlegroups.com...
> Here are 2 articles about hot peppers (capsaicin) and Ca:
> we can corelate these 2 and the result may be surprising; are you
> ready for a try out? (if you have a cold sore, open a red hot chilli
> pepper
> wipe it on the sore, then suck-up a Calcium chewable pill.
>
> 1)
>
>
http://www.jneurosci.org/cgi/conten...341fe664d52c166
5b59cfc5045c7e211b7ce17#SEC2
> Summary
>
> The results presented in this paper contribute to understanding how
> calcium feeds back to desensitize capsaicin-activated channels. The
> importance of calcium in the desensitization of capsaicin responses is
> not surprising considering the role of calcium in the desensitization
> of other receptors, including the NMDA class of the glutamate receptor
> family (Clark et al., 1990; Legendre et al., 1993) and the nicotinic
> acetylcholine receptor (Scubon-Mulieri and Parsons, 1977). The
> characterization of desensitization processes, such as those regulating
> the capsaicin response in rat DRG neurons, is crucial to understanding
> how sensory neurons can adapt their responses to repetitive stimuli in
> their environment. Furthermore, the future development and
> characterization of capsaicin analogs designed to combine increased
> desensitizing properties with decreased pungency may lead to a more
> effective therapeutic intervention for chronic pain conditions.
>
>
>
> 2)
>
> http://vir.sgmjournals.org/cgi/content/full/84/5/1071
> Capsaicin-induced reactivation of latent herpes simplex virus type 1 in
> sensory neurons in culture
>
>
> The desensitization of VR-1 at higher concentrations of capsaicin
> suggests a protective mechanism of the neuron to shut off damaging Ca2+
> influxes. Other investigators have noted desensitization of VR-1
> following repeated stimulation with capsaicin in electrophysiology
> experiments (Docherty et al., 1996; Koplas et al., 1997; Piper et al.,
> 1999). In these experiments, repeated exposure to capsaicin decreased
> and eventually abolished calcium currents. Furthermore, other studies
> have noted a decrease in mRNA levels of VR-1 following capsaicin
> treatment, suggesting down-regulation of the receptor (Mezey et al.,
> 2000). The mechanism underlying this desensitization is unknown,
> although it has been suggested that capsaicin desensitization may be
> similar to calcium-dependent inactivation of the N-methyl D-aspartate
> receptor (Docherty et al., 1996). This assumes that a particular
> threshold of intracellular Ca2+ levels negatively affects channel
> activity and gating (Koplas et al., 1997). Because capsaicin treatment
> results in rapid VR-1 desensitization in electrophysiology experiments
> and long-term desensitization in animal models, there may be two
> components of this desensitization. One component may be attributed to
> multiple ligand binding domains within particular regions on the
> receptor that change the kinetics and gating properties of the channel.
> The second component may involve receptor turnover. These two
> components may regulate the internal calcium levels to ensure survival
> of the neuron.
>
> The neuron relies on calcium channels and non-selective ion channels
> such as VR-1 to regulate intracellular calcium. Hence, VR-1 is found
> not only at the nerve terminal, but throughout the axon and soma (Guo
> et al., 1999). Additionally, the neuron expresses calcium-binding
> proteins capable of chelating excess toxic levels of calcium,
> preventing continuous stimulation and allowing cellular recovery
> (Berridge, 1998). Prolonged Ca2+ increases due to a high-intensity
> stimulus, such as a pain stimulus, causes hyperexcitation of the
> neuron. This high-intensity stimulus causes a prolonged increase in
> intracellular Ca2+, creating a wave of calcium that eventually reaches
> the soma or cell body of the neuron (Usachev & Thayer, 1999). In the in
> vitro model, this hyperexcitation may occur rapidly due to the fact
> that we are stimulating not only the nerve terminal but also the cell
> body. When hyperexcitation of a neuron occurs, these unusually elevated
> intracellular calcium levels in the soma transition the transcriptional
> machinery from a normal basal level to a highly active level (Buonanno
> & Fields, 1999; West et al., 2001). Perhaps in response to this
> increase in transcriptional activity in the neuron due to prolonged
> Ca2+ stimulation, HSV-1 is able to induce the transcription of
> immediate-early genes and begin a lytic infection. This may occur
> either via a direct role through Ca2+-dependent transcription factors
> or through an indirect activation of host-cell gene transcriptional
> machinery that serendipitously initiates HSV-1 transcription.
>
| |
| Yoshi2me 2006-10-15, 4:26 pm |
| I can think of much better things to do with a Hot Pepper! 
Angela
http://yoshi2me.com
| |
| Perl Molson 2006-10-19, 2:29 am |
|
Wanda wrote:
> Hmmm! I think if I put a hot peppr on a cold sore I might like the new sky
> light I would create!
> Wanda : )
>
Not if you hold a calcium chewable between your lips, on top of that
sore,
shortly after you used that red pepper topically.
It will stop hurting as soon as you do that.
[vbcol=seagreen]
>
>
> "Perl Molson" <beatadje@email.com> wrote in message
> news:1160640101.161340.114270@i3g2000cwc.googlegroups.com...
> http://www.jneurosci.org/cgi/conten...341fe664d52c166
> 5b59cfc5045c7e211b7ce17#SEC2
| |
| Yoshi2me 2006-10-19, 8:27 am |
| Why don't you give a whirl and let us know how it turns out for you perls.
Angela
"Perl Molson" <beatadje@email.com> wrote in message
news:1161237921.337116.57860@b28g2000cwb.googlegroups.com...
>
> Wanda wrote:
>
>
> Not if you hold a calcium chewable between your lips, on top of that
> sore,
> shortly after you used that red pepper topically.
>
> It will stop hurting as soon as you do that.
>
>
| |
| Perl Molson 2006-10-20, 2:28 am |
| Pain. 1991 Mar;44(3):301-10. Related Articles, Links
The consequences of long-term topical capsaicin application in the rat.
McMahon SB, Lewin G, Bloom SR.
Department of Physiology, St. Thomas Hospital Medical School
(U.M.D.S.), London, U.K.
Capsaicin has been used extensively as an experimental tool and in
traditional and proprietary topical medications for acute soft tissue
injuries. More recently it has been prescribed for several chronic pain
conditions where it is usually administered topically for periods of
several weeks. Here we have studied the consequences of this mode of
application in the rat. Capsaicin cream (0.075% or 0.75%), or a vehicle
cream, was applied twice daily to the hind paws of rats for a
continuous period of 10 weeks. The hind paws treated with 0.75%
capsaicin (but not 0.075%) because transiently hyperalgesic, but there
were no signs of discomfort or distress associated with the treatment.
After 10 weeks of capsaicin application, the ability of C fibres to
produce neurogenic extravasation was markedly reduced. After 4 weeks of
recovery this ability returned to normal in 0.075% capsaicin-treated
animals, but remained impaired in the 0.75% group. This latter group
showed a partial recovery 12 weeks after the end of treatment. The
levels of substance P and CGRP in the sural nerve supplying the treated
skin area were unchanged after both the 0.075% and 0.75% capsaicin
treatments. The results suggest that the topical application of
capsaicin at low concentration produces a reversible impairment of the
terminals of C fibres in the skin without greatly exciting those fibres
and without affecting the properties of cell soma. The number of
afferent neurones in the L5 dorsal root ganglion projecting through the
sural nerve was unchanged after 0.75% capsaicin treatment, suggesting
that the topical capsaicin treatment does not produce any cell death in
the adult animal.
PMID: 2052400 [PubMed - indexed for MEDLINE]
http://www.ncbi.nlm.nih.gov/entrez/...0&dopt=Abstract
Yoshi2me wrote:[vbcol=seagreen]
> Why don't you give a whirl and let us know how it turns out for you perls.
>
> Angela
>
>
> "Perl Molson" <beatadje@email.com> wrote in message
> news:1161237921.337116.57860@b28g2000cwb.googlegroups.com...
| |
| Perl Molson 2006-10-20, 2:28 am |
| http://ch-www.st-andrews.ac.uk/staf...h/capsaicin.htm
Perl Molson wrote:[vbcol=seagreen]
> Pain. 1991 Mar;44(3):301-10. Related Articles, Links
>
>
> The consequences of long-term topical capsaicin application in the rat.
>
> McMahon SB, Lewin G, Bloom SR.
>
> Department of Physiology, St. Thomas Hospital Medical School
> (U.M.D.S.), London, U.K.
>
> Capsaicin has been used extensively as an experimental tool and in
> traditional and proprietary topical medications for acute soft tissue
> injuries. More recently it has been prescribed for several chronic pain
> conditions where it is usually administered topically for periods of
> several weeks. Here we have studied the consequences of this mode of
> application in the rat. Capsaicin cream (0.075% or 0.75%), or a vehicle
> cream, was applied twice daily to the hind paws of rats for a
> continuous period of 10 weeks. The hind paws treated with 0.75%
> capsaicin (but not 0.075%) because transiently hyperalgesic, but there
> were no signs of discomfort or distress associated with the treatment.
> After 10 weeks of capsaicin application, the ability of C fibres to
> produce neurogenic extravasation was markedly reduced. After 4 weeks of
> recovery this ability returned to normal in 0.075% capsaicin-treated
> animals, but remained impaired in the 0.75% group. This latter group
> showed a partial recovery 12 weeks after the end of treatment. The
> levels of substance P and CGRP in the sural nerve supplying the treated
> skin area were unchanged after both the 0.075% and 0.75% capsaicin
> treatments. The results suggest that the topical application of
> capsaicin at low concentration produces a reversible impairment of the
> terminals of C fibres in the skin without greatly exciting those fibres
> and without affecting the properties of cell soma. The number of
> afferent neurones in the L5 dorsal root ganglion projecting through the
> sural nerve was unchanged after 0.75% capsaicin treatment, suggesting
> that the topical capsaicin treatment does not produce any cell death in
> the adult animal.
>
> PMID: 2052400 [PubMed - indexed for MEDLINE]
>
> http://www.ncbi.nlm.nih.gov/entrez/...0&dopt=Abstract
>
> Yoshi2me wrote:
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