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/content/full/17/10/3525?ijkey=72341fe664d52c1665b59
cfc5045c7e211b7ce17#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.