Like I said I am just being lazy. I have a naging question that everytime I go to look it up I get bored and start looking for something else. Mostly becuase if you type it in to pubmed you get about 10,000 hits and its hard to narow down so I am hoping one of you guys knows.

What I am wondering is the relationship to GH and prolacin. specifcially, that in normal operation you get one then you get the other. they go hand in hand. but a drug like bromocriptine, throws this out of wack. Elevating GH and reducing prolacin. does anyone know why this is specifically what area of the brain is responsible for controling this effect. I am sure the anwser is out there its just I am to lazy to look.

Per GH production: The activity of dopamine receptors in hypothalamus indicates, to certain extent, the energy state of the body. This in turn modulates GHRH production (i.e., the body likes to produce more of it if it believes there is "surplus" energy).

Per prolactinomas: I have not done that much research on this, but basically, more D2R stimulation at hypothalamus, less prolactin production. In women, this apparently gets more complicated due to estrogen.

References: The first abstract talks about dopamine agonists, prolactin, and hypothalamus. The second abstract goes into the specific areas in hypothalamus that is involved with prolactino production.

Both of the abstracts are about animal-studies, and neither of them is good for learning about the basics -- but I am lazy to search for better ones

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(1) Expression of D1 and D2 dopamine receptors in the hypothalamus and pituitary during the turkey reproductive cycle: colocalization with vasoactive intestinal peptide.

Chaiseha Y, Youngren O, Al-Zailaie K, El Halawani M.

School of Biology, Institute of Science, Suranaree University of Technology, Nakhon Ratchasima, Thailand.

The regulation of avian prolactin (PRL) secretion and PRL gene expression is influenced by hypothalamic vasoactive intestinal peptide (VIP), the PRL-releasing factor in avian species. Recent evidence indicates that D(1) and D(2) dopamine (DA) receptors play a pivotal role in VIP and PRL secretion. The differential expression of DA receptors located on hypothalamic VIP neurons and anterior pituitary cells may affect the degree of prolactinemia observed during the turkey reproductive cycle. The relative expression of D(1D) and D(2) DA receptor subtype mRNA was quantitated using in situ hybridization histochemistry (ISH). D(1D) and D(2) DA receptor mRNA was found expressed throughout the hypothalamus and pituitary. The expression of D(1D) DA receptor mRNA in the hypothalamus was found to be 6.8-fold greater than that of D(2) DA receptor mRNA. Higher D(1D) DA receptor mRNA content was found in the anterior hypothalamus (3.6-fold), the ventromedial nucleus (2.0-fold), the infundibular nuclear complex (INF; 1.9-fold), and the medial preoptic nucleus (1.5-fold) of laying hens as compared to that of reproductively quiescent non-photostimulated hens. The levels seen in incubating hyperprolactinemic hens were essentially the same as in laying hens, except for the INF where levels were 52% higher. During the photorefractory stage (hypoprolactinemia), the D(1D) DA receptor mRNA was at its lowest level in all areas tested. No differences were observed in hypothalamic D(2) DA receptor mRNA abundance throughout the reproductive cycle, except for an increase in D(2) DA receptor mRNA within the INF of photorefractory hens. Also, a marked reduction in D(2) DA receptor mRNA was observed in the pituitary of incubating hens. Pituitary D(1D) DA receptor levels did not change when birds entered the incubating phase. Double ISH revealed that D(1D) and D(2) DA receptor mRNAs were co-expressed within neurons expressing VIP mRNA, predominantly within the lateral hypothalamus and INF. D(1D) DA receptor mRNA was more highly expressed than D(2) DA receptor mRNA. The present findings clearly demonstrate that the expression of stimulatory D(1) DA receptor mRNA in the hypothalamus increases in hyperprolactinemic incubating hens, whereas inhibitory D(2) DA receptor mRNA increases in the pituitary of hypoprolactinemic photorefractory hens. Copyright 2003 S. Karger AG, Basel

(2) Quantification of prolactin-releasing peptide (PrRP) mRNA expression in specific brain regions of the rat during the oestrous cycle and in lactation.

Anderson ST, Kokay IC, Lang T, Grattan DR, Curlewis JD.

School of Biomedical Sciences, The University of Queensland, Queensland 4072, Brisbane, Australia

Real-time Taqman RT-PCR was used to make quantitative comparisons of the levels of PrRP mRNA expression in micropunch brain samples from rats at different stages of the oestrous cycle and in lactation. The nucleus of the solitary tract and ventrolateral reticular nuclei of the medulla oblongata contained significantly (P<0.05) greater levels of PrRP mRNA than any hypothalamic region. Within the hypothalamus, the highest level of PrRP expression was localised to the dorsomedial aspect of the ventromedial hypothalamus. All other hypothalamic regions exhibited significantly (P<0.05) lower levels of expression, including the rostral and caudal dorsomedial hypothalamus. Very low levels of PrRP expression were observed in the arcuate nucleus, paraventricular nucleus, medial preoptic nucleus and ventrolateral aspect of the ventromedial hypothalamus. No significant changes in PrRP expression were noted in any sampled region between proestrus, oestrus or dioestrus. Similarly, PrRP expression in hypothalamic regions did not differ between lactating and non-lactating (dioestrous) animals. During validation of RT-PCR techniques we cloned and sequenced a novel splice variant of PrRP from the hypothalamus. This variant arises from alternative splicing of the donor site within exon 2, resulting in an insert of 64 base pairs and shift in the codon reading frame with the introduction of an early stop codon. In the hypothalamus and brainstem, mRNA expression of the variant was restricted to regions that expressed PrRP. These results suggest that PrRP expression in the hypothalamus may be more widespread than previously reported. However, the relatively low level of PrRP in the hypothalamus and the lack of significant changes in expression during the oestrous cycle and lactation provides further evidence that PrRP is unlikely to be involved in the regulation of prolactin secretion.

I am quite positive that this is incorrect. It produces it when the PVN is activated. Thus the fasting induced increase in secretion.

thanks for the seconds article that was somewhat helpfull however as they also discussed in that one PrRP mRNA seems to be dosassociated with actual prolactin secretion.

That is because you are looking at "fed state" v. "fasted state"; these involve more than just dopamine releases.

As soon as you eat, because digestive organs releases hormones that modulate somatostatin (I think that is the right one), there is a delay in the release of GH until significant amount of food is processed. But this is just a delay: the increase in dopamine level is positively correlated with increase in GH, in the absense of other signaling factors.

I have two references, neither of which are too good. The first one describes a dopamine agonist and its effect on GH release.

The second one is more interesting. It talks about the intestinal release of somatostatin, which arrests the GH release. You will need to do some digging to find out when somatostatin is released from digestive organs. (I do not have the proper references at hand; and I am unable to lend a hand at the moment).

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(1) Hormonal effects of CQP 201-403, a new dopamine agonist.

Gaillard RC, Brownell J.

Departement de Medecine, University Hospital, Geneva, Switzerland.

CQP 201-403 is a propylergoline derivative with strong dopamine stimulant properties in animals models. It was developed in order to meet the need for a dopamine agonist compound which would offer longer action and improved tolerability. In this study, we tested CQP 201-403 m healthy male volunteers in order to assess its PRL suppression action and other hormonal effects as well as its duration of action and tolerability. Twenty-one volunteers participated in a dose-range study conducted according to a double-blind cross-over design with placebo control. The PRL suppression effect of single oral doses ranging from 0.05 mg to 0.035 mg were investigated. The duration of action of CQP 201-403 was tested in 6 other volunteers receiving a single oral dose of 0.025 mg or placebo. Blood was sampled over 48 h for PRL and GH measurements. An endocrine profile was performed in 6 volunteers receiving either 0.025 mg CQP 201-403 as a single oral dose or placebo. Blood was sampled over 8 h for measuring plasma PRL, GH, LH, FSH, TSH and cortisol. The results show strong dose-dependent PRL suppression (P less than 0.001) beginning 2 h after ingestion. PRL suppression lasted for more than 24 h and the normal sleep PRL surges were abolished. GH was transiently stimulated during the first few hours; the GH sleep profile was normal. All other hormones were not affected by the administration of CQP 201-403. Tolerability was good and no drug attributable changes in safety measures occurred.(ABSTRACT TRUNCATED AT 250 WORDS)

(2) [Interaction between gastrointestinal hormones and endocrine regulation]

[Article in German]

Pfeiffer EF, Raptis S, Ziegler R.

The vicinity of several hormone-producing glands as part of the anatomy of the intestinal tract and the resulting interaction has been confirmed by the discovery of hormonal factors of a specifically gastro-intestinal origin. Today we are mainly interested in the interaction between intermediary metabolism and incretory intestinal function; this is characterized by the joint action of conventional glandular hormones such as insulin and pancreatic glucagon as well as by the incretion of diffuse intestinal organs, hormones such as secretin, pancreozymin, motilin, VIP and GIP. The latter are at present subject of active research with the object of discovering their physiological significance be it as tissue hormones or as humoral agents with a "long distance" impact; their role within pathophysiology is also of interest. GIP ("gastric inhibitory peptide"), apart form acting upon the intestinal tract, also causes a marked rise in insulin production; this GIP possibly is the factor responsible for the difference in glucose tolerance following i. v. or oral administration of glucose, something that scientists have been trying to discover for a long time. We have also endeavored to investigate somatostatin. This substance was originally discovered as a hypothalamic factor with inhibitory action on growth hormone secretion; in the meantime, however, cells containing and possibly also producing somatostatin have also been detected in the intestine and particularly in the islets of Langerhans (D-cells). Since somatostatin inhibits insulin secretion and especially glucagon release as well as the exretory functions of the stomach and of the pancreas, the significance of this hormone possibly is that of a tissue hormone with inhibitory action on adjacent cells. As factor inhibiting both endocrine and exocrine secretory processes it would combine these two complexes. The possible therapeutic significance of somatostatin administration to diabetics would lie in the saving of insulin. A third sector of present-day research deals with the interaction between the calcium metabolism and the hormones involved as well as the intestine. We know that patients suffering from primary hyperparathyroidism are prone to contract stomach ulcers and pancreatitis; patients with a gastrinoma and a hyperfunction of the epithelial bodies suffer from a Zollinger-Ellison-sindrome and this again suggests association with endocrine polyadenomatosis (Wermer syndrome). The inhibitory action of the parathormone antagonist calcitonin on the exocrine functions of the intestinal tract, such as the acid secretion of the stomach and the enzyme secretion of the pancreas, have already given rise to some considerations and experiments relative to treatment. It is to be hoped that because of all the joint observations cited above there will be better intergration of research both from the aspect of gastro-enterology and endocrinology. This might hopefully elucidate some of the unresolved problems ranging from basic research to practical application.

Well, lets start with the basics of Prolactin and by doing so many questions will be answered. (I have been perplexed/intrigued by the way GH and Prolactin interact in humans in response to various stimuli for quite some time also).

Research on the effects of prolactin manipulation in males has been an area that needs much more attention IMO. Just like GH, (P) Prolactin rises in response to stress and during sleep in healthy men.

I have had my blood prolactin and GH measured several times under many diverse conditions. We know that ingestion of alcohol, morphine, estrogens, amphetamines, and benzodiazepines (valium etc) causes temporary large elevation in P secretion in healthy males. GH is also elevated in tandem with P in response to ingestion of the majority of these drugs in healthy men. Blood levels of prolactin in healthy women (not pregnant or nursing) are only 10-15% higher on average than healthy mens' P levels are. The same holds true for blood GH measurements with women having higher levels on average.

(MUCH MORE to come...)

N Engl J Med. 1982 Aug 12;307(7):444-5.

Pyridoxine (B6) suppresses the rise in prolactin and increases the rise in growth hormone induced by exercise.

Moretti C, Fabbri A, Gnessi L, Bonifacio V, Fraioli F, Isidori A.

I thought you would find the above study and its related links quite informative Spook. (Hard to believe that the NEJM would actually mention vitamin B-6 and GH/Prolactin and their relationship to intense exercise -- let alone all mentioned in one sentence! ) -- such blasphemy!

In non-lactating women, elevated P levels are very commonly linked with PMS-like symptoms. The PMS "model" is a great way to understand how P and GH interact.

In men and women, elevated P levels are almost always associated with the following hormonal abnormalities:
1- Decreased thyroid hormone activity
2- Excess estrogen/progesterone ratio - (in males also)
3- Decreased endorphin levels in the brain
4- Sub-optimal Testosterone levels
5- Elevated Aldosterone levels
6- DHEA-Sulfate deficiency
7- Reduced pulsatile LH and LH-RH levels

30-33% of the cells of the anterior pituitary gland secrete GH, while approximately 10% secrete Prolactin which is almost identical in structure to GH. If I understood the Hypothalamic-Hypophysial Portal system better, I could comment more on what I just mentioned. The very concept/notion of the "HPTA" in general is dubious the more I study the mechanisms involved...

He he. you just ran down the entire list of systems the PVN drives. But you missed one. excess cortisol, and excess epinephrine.



Seriously. I totaly agree. Its only of relevance when talking about using supraphysiological levels of steroids. I don't know how well versed you are in the different brain regions as well a the affernt nerves but I totaly agree. The more I read about the brain the less I think any of the "axis" actuall exists. it seems they only apear in ideal circumstances. particularly in light of all of the wonderfull new pseudorabies viral tracer studies. God do I love those. Its just so damn cool when you get to see exactly where nerves end up at. Oh and if you did not catch my post in another thread I am going to put a serious hurt on the notion of the HPTA in Leptin VI.

by the way, thanks for the B6 study. that is starting to somewhat anwser the origional question.

Basically what else I discovered is that L-tryptophan/5-HTP supplements dramatically elevate Prolactin levels in men when ingested orally according to several studies. Thorazine and other anti-psychotics specifically elevate prolactin levels and decrease dopamine-activity by elevating serotonin precursors in the brain.

Many studies show that acute and chronic St. Johns Wort extract ingestion in healthy men elevate serotonin levels and cortisol levels depending on the dose. In every study, prolactin/GH is either not changed, or is increased slightly during chronic-St. Johns Wort ext. ingestion in men. Clenbuterol and other beta-agonists also prevent the expected GH/Prolactin elevating effects of serotonin-ehancing drugs/supplements in healthy males - (possibly via excess cortisol/E/NE secretion from beta-agonist drug use as you suggested)...

The "TRH-challenge" test, uses synthetic TRH (thyrotropin-hormone) administered IV while Prolactin levels are monitored. Levels of Prolactin should increase 2-fold approximately in healthy men. If levels Triple after TRH is given, then the hypothalamus and/or pituitary is likely to be damaged. If Prolactin fails to increase at least 25% after the TRH stimulation test, then Hypothalamic/Pituitary damage is very likely. In other words, the thyroid gland is a key mediator of Prolactin release by the anterior Pituitary gland.

BTW, have you seen SPECT-imaging studies of the various regions of the brain? Its like watching "live-action" PET scans in humans while they are being monitored...its fascinating stuff!

Mancini A, et al. "Effects of progesterone administration on follicle-stimulating hormone and prolactin release in estrogen treated eugonadal adult men." Andrologia 1991 Sep-Oct;23(5):373-9

Bartke A, et al. "Role of prolactin in the regulation of sensitivity of the hypothalamic-pituitary system to steroid feeback." Adv Exp Med Biol 1987;219:153-75

D'Agata R, et al. "Hydrotestolactone lowers serum oestradiol and PRL levels in normal men. evidence of a role of oestradiol in prl secretion." Clin Endocrinol (Oxf) 1982 Nov;17(5):495-9

Ambrosi B, et al. "Hypothalamic-pituitary-testicular function in men with PRL-secreting tumors." J Endocrinol Invest 1981 Jul-Sep;4(3):309-15

Bartke A, et al. "Effects of physiological and abnormally elevated prolactin levels on the pituitary-testicular axis." Med Biol 1986;63(5-6):264-72

(The study below showed that excessive Prolactin decrease in healthy males causes dramatic LH increases)

Marin-Lopez G, et al. "Leydig cell function in hyper- or hypoprolactinemic states in healthy men." Invest Clin 1996 Sep;37(3):153-66

Breastfeeding is associated with blunted hypothalamic-pituitary-adrenal function and elevated prolactin synthesis. Gonadal and adrenal steroid hormone deficiency, plus elevated prolactin, facilitates the expression of Th1-type immunity.

Th2-type immunity expression correlates strongly with increased levels of corticosteroids, Prolactin, and decreased free/total testosterone levels in men.

Taurine has been shown to increase prolactin levels in nursing mothers. Taurine supps can low GA levels in the brain. The Parathyroid gland make the hormone/peptide glutataurine.

Interestingly, Taurine is a free molecule and is NEVER incorporated into muscle proteins. Since the taurine molecule is water-soluble, it doesnt cross the mostly fattly membranes in the body's cells, yet it is present in all membranes. Men also have much higher levels of the enzymes needed for taurine synthesis from cysteine than women do. This may explain the differences in prolactin levels between men and women. Taurine is also a diuretic and is very helpful for CHF by increasing sodium/water excretion. Taurine prevents potassium loss inside heart cells and is all the most abundant free amino acid in the heart.

Finally, taurine supplements can decrease elevated cortisol leves/adrenaline release while also decreasing elevated thyroxine levels in 2-4 gram doses.

Effect of melatonin on hypoglycemia and metoclopramide-stimulated arginine vasopressin secretion in normal men.
Coiro V; Volpi R; Caffarri G; Capretti L; Marchesi C; Giacalone G; Chiodera P
Department of Internal Medicine, School of Medicine, University of Parma, Italy.
Neuropeptides (Scotland) Aug 1997, 31 (4) p323-6

The present study was performed in order to establish whether melatonin (MEL) plays a role in the regulation of arginine vasopressin secretion (AVP) in normal human subjects. For this purpose, the effects of an oral administration of 6 or 12 mg MEL on basal and metoclopramide (MCP)- or hypoglycemia -stimulated AVP secretion was tested in 18 normal men. MCP was given at a dose of 20 mg as an intravenous (i.v.) bolus; hypoglycemia was induced with an i.v. bolus injection of 0.15 IU/kg body weight of insulin. In addition, in view of the well-known inhibitory effect of MEL on the growth hormone (GH) response to hypoglycemia, GH levels were measured during the insulin tolerance test (ITT), as an independent index of MEL activity. MEL did not produce any change in AVP secretory patterns in basal conditions or during the MCP test. In contrast, the mean peak AVP response to hypoglycemia was 2.33 times higher than baseline in the control ITT, whereas it was only 1.77 times higher than baseline in the ITT plus MEL tests. Also, the GH response to hypoglycemia was significantly lower in the presence than in the absence of MEL. For both AVP and GH, the inhibitory effect of MEL during ITT was similar, when either 6 or 12 mg MEL was given. These data indicate an involvement of MEL in the control of the AVP response to hypoglycemia, but not of basal and MCP-induced AVP secretion. In addition, the similar effects of MEL on GH and AVP secretions during ITT suggest that similar neuroendocrine mechanisms underlie these hormonal responses to hypoglycemia.

The above suggests that Reglan - the commonly prescribed anti-nausea drug ALSO increases GH levels in conjunction with its well known Prolactin stimulating effects (the correlation spook mentioned).
We know that Reglan is also a VERY potent dopamine receptor antagonist. Reglan is well known to stimulate Vasopressin release when taken orally in 15mg+ doses.

Once again, blood glucose manipulation is a potent variable that can be manipulated to increase Vasopressin release. Vasopressin release is also stimulated by acetylcholine agonists which partially may explain its potent memory enhancing effects in humans. Reglan is also well known to stimulate aldosterone and thyrotropin release which is directly related to Prolactin secretion also. Melatonin we see is definitely involved in glucose homeostasis at doses 6mg and over. Another reason why high-dose melatonin supplementation can be detrimental due to its strong GH- inhibiting effects. Another good reason why melatonin supps should be cycled on and off and used in doses less than 6 mg in most men...

I am just starting to research (during times I need a break from other research) Prolactin, dopamine and it's effects on Male Libido.

It seems a combination of Dopamine agonists and Prolactin inhibitors enable men to succesfully copulate again just a few minutes after first orgasm. Though there is a study showing an increase in Prolactin during sexual excitement and orgasm, they did not say how close to orgasm the measurements were taken. It looks as if Prolactin is released in large amounts around orgasm time (probably in conjunction with large release of dopamine.)

Anyway, the reason I am looking at this is when I am on cycle, I have a huge problem with my libido disappearing. I also have this problem due to depression (though Wellbutrin, a dopamine reuptake inhibitor, seems to help).

Interestingly enough, two different herbs I had taken a look at that have been used for centuries as aphrodisiacs are showing an inhibitory effect of Prolactin. I have contacted a chinese herb company I used to work for, as when I had experimented 12 years ago with onje of these herbs, I noticed VERY dramatic effects on both libido and semen output (it is said that Prolactin has a "drying" effect on the prostate).

Anyone interested in this area besides me?

I plan to play a bit - manipulating Dopamine levels and supress Prolactin? I'll keep you updated.

......

Bump.
Vitex (without a bunch of isoflavines!), ldopa, what else?

abstince is actually teh best hting ever for your prolactin. that and sleep.

Yeah, but if there are two things I feel are a waste of life it's sleep and abstinence

HA! Well said

Ahhh...but what if one is prone to wet dreams?

pfft masturbation.

Well, is it still masturbation if you don't use your hands?