09-25-2010, 07:39 AM
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Join Date: Mar 2010
| | Re: What is the correlation between testosterone and dopamine?
Originally Posted by m_ob
so could it be possible that testosterone
increases dopamine ( higher test
higher dopamine levels), but higher levels of test
increase estrogen to such levels that the dopamine increase can not make up for the prolactin increase do to estrogen increase...but testosterone increase without estrogen increase decreases prolactin via the dopminergic route?
this stament is coherent?
Looks like very interesting hypothesis.. But I think this has more to do with testosterone metabolites: DHT
- affect CNS
estradiol works as MAOI - enhances neurotransmitters influence
High estradiol can elevate prolactin.
It's interesting if DHT
can lower estradiol, prolactin and increase dopamine..?
Estradiol-induced prolactinomas: differential effects on dopamine in posterior pituitary and median eminence |
References and further reading may be available for this article. To view references and further reading you must purchase this article.
Richard A. Burgetta, Paul A. Garrisa and Nira Ben-JonathanCorresponding Author Contact Information, a
aDepartment of Physiology and Biophysics, Indiana University School of Medicine, Indianapolis, IN 46223, U.S.A.
Accepted 24 April 1990.
Available online 10 March 2003.
Prolactin release is inhibited by dopamine and stimulated by estradiol. Dopamine is released from nerve terminals in the median eminence and posterior pituitary. Estradiol may act directly on the anterior pituitary or by modulating the two dopaminergic systems. Estradiol treatment induces the formation of prolactinomas in Fischer 334 rats. Therefore, this strain was chosen as the experimental model. The first objective was to determine whether estradiol differentially regulates the two dopaminergic systems. The second objective was to explore whether the anterior pituitary in estradiol-treated rats acquires the capability for de novo synthesis of dopamine. Rats were ovariectomized and implanted with estradiol capsules (OVEX + E2). Controls were untreated ovariectomized rats (OVEX). Three weeks thereafter, rats were killed. Anterior and posterior pituitaries and medial basal hypothalami (MBH) were removed and individually incubated for 60 min in Hank's balanced salt solution containing 10 μCi [3H]-tyrosine. The median eminence was then dissected from the MBH. Tissues were homogenized in perchloric acid and the supernatant fluids were extracted with alumina. Both endogenous and tritiated dopamine were simultaneously quantitated by HPLC. Prolactinoma formation in OVEX + E2 rats was confirmed by dramatic rise (50-fold) in plasma prolactin levels and marked enlargement (3-fold) of the anterior pituitary. Estradiol treatment caused a significant 60% reduction in both dopamine content and synthesis in the median eminence. In contrast, estradiol treatment affected neither dopamine content nor synthesis in the posterior pituitary. There was no evidence for de novo synthesis of dopamine in anterior pituitaries from either OVEX or OVEX + E2 rats. We conclude that the two dopaminergic systems which regulate prolactin secretion, exhibit a differential response to estradiol.
Keywords: Prolactinoma; Estradiol; Dopamine; Posterior pituitary; Stalk-median eminence
Endocrinology. 1992 Jul;131(1):395-9. |
Role of dopamine in the regulation of gonadotropin-releasing hormone in the male rat brain as studied by in situ hybridization.
Li S, Pelletier G.
MRC Group in Molecular Endocrinology, CHUL Research Center, Quebec, Canada.
The effects of the dopaminergic antagonist haloperidol (HAL) as well as the D2 dopamine receptor agonist bromocriptine (BRO) on GnRH messenger RNA (mRNA) levels in the male rat were investigated by quantitative in situ hybridization. Since it had already shown that androgens could induce a decrease in GnRH mRNA levels in castrated rats, the involvement of the dopaminergic system in the inhibitory effect of dihydrotestosterone (DHT) was also investigated. In situ hybridization was performed on paraformaldehyde-fixed cryostat sections through an area extending from the preoptic area to the anterior hypothalamus using a 35S-labeled 48-base oligodeoxynucleotide complementary to the GnRH coding region of the GnRH DNA. The corresponding mRNA levels were assessed by counting the number of silver grains overlying labeled neurons. In intact animals, a 14-day treatment with BRO increased by 67% the number of silver grains per neuron while HAL decreased by 31% the value of this parameter. Hypophysectomy which induced a 22% decrease in the hybridization signal could not prevent the effects of BRO or HAL. Gonadectomy performed 14 days earlier increased by 54% the mean number of silver grains while a 14-day treatment of gonadectomized animals with DHT decreased the hybridization signal by 48%. On the other hand, the concomitant administration of HAL and DHT did not prevent the inhibitory effect of DHT but rather resulted in a decrease of the hybridization signal which was more marked than that induced by DHT or HAL alone. The present data clearly demonstrate that GnRH mRNA levels are positively regulated by dopamine and that the effects of BRO and HAL on GnRH mRNA are not mediated by variations in pituitary hormone secretion. Moreover, our results suggest that the effect of DHT on GnRH gene expression is probably not mediated by the dopaminergic system.
PMID: 1612019 [PubMed - indexed for MEDLINE]
Get healthy level of androgens or die trying..