Anyone thats seen a few of my recent posts probably knows where im going with this. This could be one of those compensatory mechanisms.
Right here im thinking histamine. Someone else said they associated this scalp itch with recovery.
I dont claim to have this figured out, but from what ive been looking at, no single molecule might be involved in more functions then histamine. Good or bad, this maybe should be kept in mind.
EFFECT OF A GONADOTROPIN-RELEASING HORMONE ANALOGUE ON
TESTICULAR AND PERITONEUM HISTAMINE CONCENTRATION IN
PUBERTAL MALE RATS
Gonadotropin releasing hormone agonist (GnRH-A) at supraphysiological doses
and chronically administrated has been utilized for several clinical applications,
including the treatment of prostate cancer (PC) in men and central precocious puberty
(CPP) in boys (Wilson et al., 2007). In other male mammals species, a chronic
administration of GnRH-A has been tested, as in dogs (Vickery et al., 1985; Trigg et al.,
2001), cheetahs (Bertschinger et al., 2006), bulls (D’Occhio et al., 2000), ferrets
(Schoemaker et al., 2008) monkeys (Lunn et al., 1992) and wallabies (Herbert et al.,
2004) as an alternative for surgical castration
GnRH-A treatment associated with androgen
replacement produced a dramatic increase in testicular histamine concentration, which
was markedly greater than the increase produced by the treatment with GnRH-A only.
Peritoneum histamine concentration was not affected by GnRH-A treatment. These
results demonstrate that the effect of GnRH-A in increasing testicular histamine
concentration in pubertal male rats, is potentiated by testosterone. Since mast cells and
histamine seem to have an important role in the restoration of testis function, the
increase of testicular histamine concentration after GnRH-A treatment may be an
adaptive response of testis to the impairment of steroidogenesis.
As we have observed, the treatment with GnRH-A impairs testicular
steroidogenesis and results in a significantly lower production of testosterone. The
increase of testicular histamine concentration after treatment with GnRH-A may be an
adaptive response of testis to the impairment of steroidogenesis.
These data clearly indicate that mast cells and histamine can modulate Leydig
cell steroidogenesis and have an important role in the restoration of testis function.
In our results, we have observed that the treatment with GnRH-A only caused
low testicular testosterone concentrations and elevated testicular histamine levels. As we
discussed previously, the effect caused after GnRH-A treatment, increasing the testicular
histamine concentration may be a compensatory response of testis to the impairment of
steroidogenesis. In this case, the increase in the testicular histamine concentration would
be a secondary response to the reduction of the local testosterone production. Since the
inhibitory effect of GnRH-A on testis function (spermatogenesis and steroidogenesis) is
reversible with the suspension of therapy both in CP and CPP in humans it is possible to
postulate a participation of histamine in testicular function restoration. However, we also
observed that the treatment of GnRH-A associated with testosterone propionate led to a
dramatic increase in testicular histamine concentration associated with a higher testicular
testosterone concentration. This result raises the possibility that the increase of testicular
histamine concentration after GnRH-A treatment may not be simply a secondary
response to the impaired testicular steroidogenesis. It is possible that both GnRH-A and
testosterone directly stimulate testicular mast cells and histamine production