Accidental capsaicin on penis,,,please help!

Lurker me at
Fri Sep 5 19:13:37 EST 2003

About 5 months ago my not-so-bright at the time gf decided to try to help me
with my impotence problem(I am 36) by chopping up jalapenos and masturbating
me. Well my fellow was very wam---not burning--but warm. I washed it
thourghly with soap and water and only found out the next day I needed to
put milk on it. I have since lost sensitivity--or so I think(I am under
tremendous stress as well). I have found some links stating that capsaicin
will kill the nerves if left on over two hours---is that true? Did I get
enough dose? Will the receptors regenerate? I am so seriously stressed about
this---comments and help please. Thanks!

The capsaicin receptor: a heat-activated ion channel in the pain pathway."
The focus, Capsaicin, is a molecule found in the white "ribs" of hot peppers
that is the root of our perception of heat from the peppers. It is assumed
to be a defense mechanism in a variety of pepper plants. The capsaicin found
in hot peppers work by binding to and stimulating capsaicin receptor
proteins found in neuronal cells. The fibers of the neuronal cells then
carry the stimulus from areas such as the tongue, to the roots of the spinal
cord. Capsaicin also allows a deluge of calcium ions to enter the neuron.
This is dangerous, because an extended exposure to calcium causes the fibers
of the neuron to die.

The Summary of "The capsaicin receptor: a heat-activated ion channel in the
pain pathway"
Capsaicin is a natural product of capsicum peppers, that is an active
ingredient in many hot foods. When nociceptors- neurons that transmit
information regarding tissue damage to pain-processing centers in the spinal
cord and brain- come in contact with capsaicin, the neuron gets excited, and
there is a perception of pain, and the a local release of inflammatory
mediators. These nociceptors get excited by increasing permeability of
plasma membrane to cations, but the molecular mechanism explaining this
phenomenon is unclear. Capsaicin is being used in an analgesic agent in the
treatment of painful disorders, causing long-term loss of responsiveness
because it kills off the nociceptor, or it destroys the peripheral
terminals. It was decide that the existence of a receptor site represents
the most likely mechanism, because the capsaicin derivative showed
structure-function relationships and evoked responses in a dose-dependent
manner. A competitive capsaicin antagonist called capsazepine strengthened
this model, along with discovering resiniferatoxin, an extremely potent
capsaicin analogue for Euphorbia plants that mimics the cellular action of
capsaicin. The cloning of a gene encoding a capsaicin receptor was decided
to help develop more understanding of the molecular nature of capsaicin
action and its relationship to endogenous pain signaling mechanisms. A cDNA
clone that reconstitutes capsaicin responsiveness in non-neuronal cells was
isolated. It was discovered that capsaicin gives off burning sensations
through the activation of a heat-gated ion channel that is likely to
contribute to the detection of painful thermal stimuli in vivo. Since the
molecular structure of capsaicin receptors was not known, the experimenters
adopted a functional screening strategy for isolating candidate cDNA clones.
Because capsaicin has the ability to trigger robust calcium influx into
sensory neurons in vitro, a cloning strategy was contrived. Since capsaicin
responsiveness seemed to be confined to nociceptive neurons with cell bodies
that resided within sensory ganglia, a cDNA library was constructed from
dorsal root ganglion-derived messenger RNA. The pools consisted of 16,000
clones in each, and was transfected in human embryonic kidney-derived
HEK193, and the transfected cells were filled with the fluorescent
calcium-sensitive dye Fura-2 (emits light when in contact with Calcium), and
examined for capsaicin-evoked changes in intracellular calcium levels. When
a positive pool was found, it was reassayed, repeating the process over and
over, until an individual clone containing a 3-kilobase cDNA insert was
weeded out, which conferred capsaicin or resiniferatoxin. It was determined
that this was the DNA-encoded aminoacid sequence of the protein that
comprises the capsaicin receptor. Since the vanilloid group chemically
represents capsaicin, it was called VR1. The scientists compared the
pharmacological properties of the cloned receptor to those of native
vanilloid sites in sensory ganglia. They examined the electrophysiological
responses to a variety of vanilloid agonaists and antagonists. It was
concluded that capsaicin and resiniferatoxin activate the current, while
capsazepine, and synthetic antagonist, blocks the current. It was suggested
that there is more that one binding site for the agonists molecule, which is
true with vanilloid receptors. Capsaicin is able to bind to a channel form
either the exterior or the interior of the plasma membrane. It was
discovered that the cell lines made to express VR1 die after several hours
of continuous exposure to capsaicin. The reason seems to be because of
injury, and the researchers think it is induced by the continuous influx of
ions. The reason for the death of cells when capsaicin is present in the
cell, is because the capsaicin opens the ion channel, letting calcium in.
When too much Calcium is let in, the cells die. It was suggested that
vanilloid receptors serve as specific molecular markers for nociceptive
neurons. Trigeminal and dorsal root sensory ganglia contain
capsaicin-sensitive neurons. They were not found in the spinal cord or
brain. Two other tissues that have been proposed to express capsaicin
receptors are the nodose ganglion and the preoptic area of the hypothalamus.
There was no detection of VR1 expression at these location, but vanilloid
responsiveness here might be conferred by distinct VR1 subtypes. There was a
hypothesis that VR1 is activated by noxious heat, and not innocuous heat. It
was found that rapid increases in temperature evoke ion currents from
expressed VR1 channels that closely mimic those induced by capsaicin.
Therefore the hypothesis was supported by the results.

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