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That's another why through which T increases social status!Testosterone increases dopamine through D2
Nice. What’s some of the strongest D2 agonists (as I’m also looking to lower prolactin)Dopamine causes weight loss through D1, D5 and D2 . Through different mechanisms though :
D1 and D5 = increase in adiponectin and decrease in leptin
D2 = prolactin decrease
"DAR are variably expressed at the mRNA and protein levels in adipose tissue and adipocytes during adipogenesis. ARSA activity in adipocyte increases after differentiation. DA at nM concentrations suppresses cAMP, stimulates cGMP, and activates MAPK in adipocytes. Acting via D2R-like receptors, DA and DA-S inhibit PRL gene expression and release. Acting via D1R/D5R receptors, DA suppresses leptin and stimulates adiponectin and IL-6 release."
(Dopamine receptors in human adipocytes: expression and functions - PubMed)
I'm not sure, but I dont think cabergoline improves dyskinesia through downregulation of D2 receptors. If that was true cabergoline would just stop working for prolactinoma after a few weeks, yet most people are on it for months, years or even decades . And it works, as long as they're on the drug.Isn't increase in dopamine will eventually cause a downregulation/desensitization of dopamine receptors ? The same, opposite way, like antipsychotics causing an increase in D2 density, by blocking dopamine. This is a possible mechanism of paradoxical dopamine supersinsitivity syndrome and tardive dyskinesia after withdrawal. And D2 agonist like cabergoline , prevents dyskinesia. (logically by downregulating D2 eventually)
Chronic haloperidol administration increases the density of D2 dopamine receptors in the medial prefrontal cortex of the rat - Psychopharmacology
Rats received haloperidol (1.3–1.5 mg/kg/day) via their drinking water for 21 weeks. At the end of this period the density of D2 dopamine receptors and their affinity for [3H]-spiperone were measured in the striatum and medial prefrontal cortex. The chronic haloperidol treatment increased the...link.springer.com
Sustained cabergoline treatment reverses levodopa-induced dyskinesias in parkinsonian monkeys - PubMed
The pathophysiology of L-Dopa-induced dyskinesias (LID), a common problem after long-term use of L-dopa in the treatment of Parkinson's disease (PD), is not completely understood. Oscillations in L-Dopa concentrations in the brain are believed to be responsible, at least in part, for their...pubmed.ncbi.nlm.nih.gov
I'd say cabergoline or bromocriptine. Lisuride to a lesser extent.Nice. What’s some of the strongest D2 agonists (as I’m also looking to lower prolactin)
To go full circle here : serotonin decreases social statusThat's another why through which T increases social status!
Press releases | Elsevier
Press release news service - Full overview of the main news and business updates.www.elsevier.com
D2 receptor exists in sperm as well. Implicated in sperm health and fertility. Maybe that's why selegiline and bromocriptine have been shown to help with fertility.These studies show that the Dopmine D2 receptors are strongly involved in obesity and insulin resistance .
1. (Brain dopamine and obesity - PubMed)
"Striatal dopamine D2 receptor availability was significantly lower in the ten obese individuals (2.47 [SD 0.36]) than in controls (2.99 [0.41]; p < or = 0.0075). In the obese individuals body mass index (BMI) correlated negatively with the measures of D2 receptors (r=0.84; p < or = 0.002); the individuals with the lowest D2 values had the largest BMI. By contrast, neither whole brain nor striatal metabolism differed between obese individuals and controls, indicating that striatal reductions in D2 receptors were not due to a systematic reduction in radiotracer .
2. (Low dopamine striatal D2 receptors are associated with prefrontal metabolism in obese subjects: possible contributing factors - PubMed)
"We had previously documented a reduction in dopamine D2 receptors in morbidly obese subjects."
"In obese subjects striatal D2 receptor availability was lower than controls and was positively correlated with metabolism in dorsolateral prefrontal, medial orbitofrontal, anterior cingulate gyrus and somatosensory cortices."
"The associations between striatal D2 receptors and prefrontal metabolism in obese subjects suggest that decreases in striatal D2 receptors could contribute to overeating via their modulation of striatal prefrontal pathways, which participate in inhibitory control and salience attribution. "
3. Last but not least, there is this book by lyle Macdonald on bromocriptine ,which explains the mechanism of D2 agonism and increased insulin /leptin sensitivity very well .
(Awesome Bromocriptine Book By Lyle Mcdonald)
This study has the same conclusion as the book : "...diminished insulin sensitivity is related to less endogenous dopamine at dopamine D2/3 receptor in the ventral striatum."
(Reduced insulin sensitivity is related to less endogenous dopamine at D2/3 receptors in the ventral striatum of healthy nonobese humans - PubMed)
So dopamin D2 agonism seems important to keep insulin sensitivity , lower /adequate appetite and in generel a lower body weight.
Besides that this the MoA through which bromocriptine lowers prolactin , and increases insulin and leptin sensitivity .
Btw, cyproheptadine is a D2 receptor antagonist . Many people claim the antagonism isn't significant , but if the antagonism isn't enough to matter, then how come cypro has increased appetite and weight gain as side effects .
The exact things that D2 antagonism causes!
I do think it's a great anti-stress tool ,but this shouldn't be ignored/ kept in mind when taking it. .
I know this only kind of answers your question, but I thought it was interesting and quite unique .Isn't increase in dopamine will eventually cause a downregulation/desensitization of dopamine receptors ? The same, opposite way, like antipsychotics causing an increase in D2 density, by blocking dopamine. This is a possible mechanism of paradoxical dopamine supersinsitivity syndrome and tardive dyskinesia after withdrawal. And D2 agonist like cabergoline , prevents dyskinesia. (logically by downregulating D2 eventually)
Chronic haloperidol administration increases the density of D2 dopamine receptors in the medial prefrontal cortex of the rat - Psychopharmacology
Rats received haloperidol (1.3–1.5 mg/kg/day) via their drinking water for 21 weeks. At the end of this period the density of D2 dopamine receptors and their affinity for [3H]-spiperone were measured in the striatum and medial prefrontal cortex. The chronic haloperidol treatment increased the...link.springer.com
Sustained cabergoline treatment reverses levodopa-induced dyskinesias in parkinsonian monkeys - PubMed
The pathophysiology of L-Dopa-induced dyskinesias (LID), a common problem after long-term use of L-dopa in the treatment of Parkinson's disease (PD), is not completely understood. Oscillations in L-Dopa concentrations in the brain are believed to be responsible, at least in part, for their...pubmed.ncbi.nlm.nih.gov