Dopamine, Prolactin and Oxytocin

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[Questions from a reader, and answers from Gary Wilson]

1. It appears there is a relatively inverse relationship between
dopamine levels and prolactin levels. Is that correct?

In a way. Dopamine is the major neurotransmitter that puts the brakes on prolactin secretion. However like all hormones there are many factors and other hormones involved in its secretion.

2. Assuming this inverse relationship, how do the hormone levels
self-regulate? Is one hormone a "master" and the other the "slave"
mirroring the level of the "master"? Or is there some other mechanism?

With over 200 hormones and signaling molecules, there are no masters and slaves, only interrelationships. There are multiple and extremely complex mechanisms for hormones circulating in the blood. Not only the levels of a single hormone influences body functions, but the precise levels of all other hormones at that moment that affect the potency of the aforementioned hormone. And there are yet alternative mechanisms for hormones levels in each part of the brain. And yet different mechanisms for hormones secreted to neighboring cells. There are also hormones secreted that in turn affect the cell that secreted the hormone.

3. If, for example, there is a master-slave relationship and dopamine
is the "master", what triggers changes in dopamine levels besides
orgasm? It would appear that dopamine level can be artificially
triggered to increase by engaging in specific behaviors (sex, shopping,
eating, etc.). Thus, dopamine level could be regulated to an extent by
consciously engaging or not engaging in certain activities. Is this
true?

This is very true, except the part about master-slave.

4. What is the effect of oxytocin on dopamine-prolactin levels? Is
there a relationship or is oxytocin level independent of the
dopamine-prolactin balance? My experience has been that prolonged,
relaxed foreplay (presumably increasing oxytocin levels) prior to
traditional sex and orgasm has at least two effects. First, a greater
sense of well being instead of exhaustion following orgasm. And,
second, less desire for separation for 24-36 hrs. afterward (sense of
closeness, more forgiving/easier to get along with, desire for
monogamy, wife looks better, fewer cravings, etc.). I'm wondering if
the oxytocin actually alters the dopamine-prolatin levels or merely
masks their effects. What would the oxytocin level look like if plotted on your dopamine-prolactin chart? Might it look like this? Or
are the dopamine & prolactin levels impacted in some way?

Sometimes oxytocin increases dopamine, sometimes it decreases dopamines. Often Oxytocin increases dopamine, but under certain circumstances it decreases dopamine. Nothing is independent when it comes to hormones.

ABSTRACT

Cannabis (i.e., marijuana and cannabinoids) is the most commonly used illicit drug in developed countries, and the lifetime prevalence of marijuana dependence is the highest of all illicit drugs in the United States. To provide clues for finding effective pharmacological treatment for cannabis-dependent patients, we examined the effects and possible mechanism of lithium administration on the cannabinoid withdrawal syndrome in rats. A systemic injection of the mood stabilizer lithium, at serum levels that were clinically relevant, prevented the cannabinoid withdrawal syndrome. The effects of lithium were accompanied by expression of the cellular activation marker Fos proteins within most oxytocin-immunoreactive neurons and a significant increase in oxytocin mRNA expression in the hypothalamic paraventricular and supraoptic nuclei. Lithium also produced a significant elevation of oxytocin levels in the peripheral blood. We suggest that the effects of lithium against the cannabinoid withdrawal syndrome are mediated by oxytocinergic neuronal activation and subsequent release and action of oxytocin within the CNS. In support of our hypothesis, we found that the effects of lithium against the cannabinoid withdrawal syndrome were antagonized by systemic preapplication of an oxytocin antagonist and mimicked by systemic or intracerebroventricular injection of oxytocin. These results demonstrate that oxytocinergic neuronal activation plays a critical role in the action of lithium against the cannabinoid withdrawal syndrome in rats, thus providing a potentially novel strategy for the treatment of cannabis dependence in humans.

Here are some interesting abstracts about recent research in this area. Also see our article: http://www.reuniting.info/RAsexbrain.htm

OXYTOCIN AND ADDICTION: A REVIEW
by
Kovacs GL, Sarnyai Z, Szabo G
Central Laboratory,
Markusovszky Teaching Hospital, Hungary.
glkovacs@mail.matav.hu
_PSYCHONEUROENDOCRINOLOGY_ 1998 NOV; 23(8):945-62

Neuropeptides affect adaptive central nervous system processes
related to opiate ethanol and cocaine addiction. Oxytocin (OXT), a
neurohypophyseal neuropeptide synthesized in the brain and released
at the posterior pituitary, also is released in the central nervous
system (CNS). OXT ACTS WITHIN THE CNS AND HAS BEEN SHOWN TO INHIBIT
THE DEVELOPMENT OF TOLERANCE TO MORPHINE, AND TO ATTENUATE VARIOUS
SYMPTOMS OF MORPHINE WITHDRAWAL IN MIce. IN RATS, INTRAVENOUS
SELF-ADMINISTRATION OF HEROIN WAS POTENTLY DECREASED BY OXT
TREATMENT. IN RELATION TO COCAINE ABUSE, OXT DOSE-DEPENDENTLY
DECREASED COCAINE-INDUCED HYPERLOCOMOTION AND STEREOTYPED GROOMING
BEHAVIOR. FOLLOWING CHRONIC COCAINE TREATMENT, THE BEHAVIORAL
TOLERANCE TO THE SNIFFING-INDUCING EFFECT OF COCAINE WAS MARKEDLY
INHIBITED BY OXT. Behavioral sensitization to cocaine, on the other
hand, was facilitated by OXT. OXT RECEPTORS IN THE CNS--MAINLY THOSE
LOCATED IN LIMBIC AND BASAL FOREBRAIN STRUCTURES--ARE RESPONSIBLE FOR
MEDIATING VARIOUS EFFECTS OF OXT IN THE OPIATE- AND COCAINE-ADDICTED
ORGANISM. DOPAMINERGIC NEUROTRANSMISSION--PRIMARILY IN BASAL
FOREBRAIN STRUCTURES--IS ANOTHER IMPORTANT BIOCHEMICAL MEDIATOR OF
THE CENTRAL NERVOUS SYSTEM EFFECTS OF OXT. TOLERANCE TO ETHANOL (E.G.
HYPOTHERMIA-INDUCING EFFECT OF ETHANOL) ALSO WAS INHIBITED BY OXT.

OXYTOCIN AS A POSSIBLE MEDIATOR OF SSRI-INDUCED ANTIDEPRESSANT
EFFECTS.

Uvnäs-Moberg K, Bjökstrand E, Hillegaart V, Ahlenius S.

_PSYCHOPHARMACOLOGY (BERL). 1999 FEB;142(1):95-101. _

Department of Physiology and Pharmacology, Karolinska Institute,
Stockholm, Sweden.

The nonapeptide oxytocin is released into systemic circulation in
situations of psychosocial interaction, and has been shown to be
involved in mechanisms of social bonding and social recognition in
laboratory studies. In view of disturbances in psychosocial
relationships being a triggering factor for depression and anxiety,
it is interesting to note that experimental studies have shown
oxytocin to possess antidepressant- and anxiolytic-like actions.
Thus. in the present study we examined effects of the SSRI citalopram
(20 mg/kg i.p.) on plasma oxytocin, acutely and upon repeated
administration, in adult male Sprague-Dawley rats. Plasma oxytocin,
and some functionally related peptides (CCK, gastrin, somatostatin
and insulin), were measured by standard radioimmunoassay techniques.
Acute citalopram administration produced a statistically significant
increase in plasma oxytocin and CCK levels. Administration of
citalopram for 14 days did not attenuate the oxytocin-releasing
effect to a challenge dose of the SSRI zimeldine (20 mg/kg s.c.),
whereas CCK levels were not increased after the subchronic citalopram
treatment. Thus, the SSRI citalopram produces increased plasma
oxytocin levels acutely, and there appears to be no or little
tolerance to this effect upon repeated administration. There were no,
or variable, effects on plasma levels of gastrin, somatostatin or
insulin. IT IS SUGGESTED THAT OXYTOCIN RELEASE IS AN IMPORTANT ASPECT
OF THE PHARMACOLOGICAL ACTIONS OF SSRIS, AND THIS COULD BE AN
IMPORTANT CONTRIBUTORY FACTOR FOR THE CLINICAL PROFILE OF THIS GROUP
OF ANTIDEPRESSANTS WITH PARTICULAR EFFICACY IN DISORDERS OF
PSYCHOSOCIAL ORIGIN.

ROLE OF OXYTOCIN IN THE NEUROADAPTATION TO DRUGS OF ABUSE
by
Sarnyai Z, Kovacs GL
Alcohol and Drug Abuse Research Center,
Harvard Medical School-McLean Hospital,
Belmont, MA 02178, USA.
_PSYCHONEUROENDOCRINOLOGY_ 1994; 19(1):85-117

Oxytocin (OXT), a neurohypophyseal hormone, has a wide range of
behavioral effects outside its classic peripheral endocrine
functions. OXT involvement in adaptive central nervous system
processes has been demonstrated as an inhibitory, amnestic action on
learning and memory in different paradigms. Because adaptation and
learning are likely to be involved in the neural events leading to
drug tolerance and dependence, the question logically arose whether
OXT is able to influence the development of tolerance of and
dependence on abused drugs. In this review, we summarize our results
on the effects of OXT on opiate (including morphine, heroin, and the
endogenous opiates beta-endorphin and enkephalin) tolerance and
dependence, heroin self-administration, psychostimulant-induced
behavioral changes, and behavioral tolerance and sensitization. The
sites and mechanisms of action and the possible physiological role of
OXT are also discussed. In the first part of this review the effects
of exogenously administered OXT on both the acute and chronic
behavioral effects of opiates and psychostimulants have been
summarized. OXT inhibited the development of tolerance to morphine,
heroin, beta-endorphin, and enkephalin, OXT also inhibited the
development of cross-tolerance between the predominantly mu-agonist
heroin and the predominantly delta-agonist enkephalin in mice.
Naloxone-precipitated morphine withdrawal syndrome was also
attenuated by OXT. Heroin self-administration was decreased by OXT
administration in heroin-tolerant rats. OXT inhibited cocaine-induced
exploratory activity, locomotor hyperactivity, and stereotyped
behavior in rats and in mice. Behavioral tolerance to cocaine was
also attenuated by OXT. On the contrary, OXT stimulated the
development of behavioral sensitization to cocaine. OXT did not alter
the stereotyped behavior induced by amphetamine. In the second series
of experiments, the sites of action of OXT on drug-related behavior
were investigated. Intracerebro-ventricular (ICV) and intracerebral
(IC) administration of an OXT-receptor antagonist inhibited the
effects of peripherally administered OXT on morphine tolerance,
heroin self-administration, and cocaine-induced sniffing behavior.
This suggests the central, intracerebral location of OXT target
sites. Local IC microinjection of OXT in physiological doses into the
posterior olfactory nucleus, tuberculum olfactorium, nucleus
accumbens, central amygdaloid nucleus, and the hippocampus inhibited
the development of tolerance to and dependence on morphine as well as
cocaine-induced sniffing behavior and tolerance to cocaine. The
physiological role of endogenous OXT in acute morphine tolerance has
also been demonstrated, since OXT antiserum (ICV) and OXT-receptor
antagonist (injected into the basal forebrain structures) potentiated
the development of morphine tolerance. Finally, we investigated the
possible mechanisms of action of OXT on drug related behavior. Both
morphine tolerance and dependence, and cocaine administration,
increased dopamine utilization in the mesencephalon and in the
nucleus accumbens, respectively. OXT treatment decreased the
alpha-methylparatyrosine-induced dopamine utilization in the
mesencephalon and in the nucleus accumbens-septal complex. Chronic
OXT treatment decreased the number of apparent binding sites of
dopamine in the basal forebrain area. It also inhibited a
cocaine-induced increase in dopamine utilization in the nucleus
accumbens, but not in the striatum. In light of this information, it
appears that OXT inhibits the development of opiate tolerance,
dependence, and self-administration as well as the acute behavioral
actions of and chronic tolerance to cocaine. This suggests the
possible role of this neuropeptide in the regulation of drug abuse.
Therefore, OXT may act as a neuromodulator on dopaminergic
neurotransmission in limbic-basal forebrain structures to regulate
adaptive CNS processes leading to drug addiction.

ACUTE COCAINE ALTERS OXYTOCIN LEVELS IN THE MEDIAL PREOPTIC AREA
AND AMYGDALA IN LACTATING RAT DAMS: IMPLICATIONS FOR COCAINE-INDUCED
CHANGES IN MATERNAL BEHAVIOR AND MATERNAL AGGRESSION.

Elliott JC, Lubin DA, Walker CH, Johns JM.

_NEUROPEPTIDES_. 2001 APR;35(2):127-34.

Department of Psychology, University of North Carolina at Chapel
Hill, NC 27599-3270, USA. jce@email.unc.edu

Acute cocaine administration has been correlated with disruptions
in the onset and maintenance of maternal behavior as well as
decreases in maternal aggressive behavior in rat dams. A GROWING BODY
OF EVIDENCE SUGGESTS THAT COCAINE MAY ALTER OXYTOCIN LEVELS LEADING TO
IMPAIRMENTS IN MATERNAL BEHAVIOR AND AGGRESSION. The current study
assessed whether acute cocaine injections alter oxytocin (OT) levels
in the medial preoptic area (MPOA), ventral tegmental area (VTA),
amygdala (AMY), and hippocampus (HIP) on postpartum day (PPD) 1 or
PPD 6. On PPD 1, 30 mg/kg cocaine reduced OT levels by approximately
26.9% (picograms/milligram) in the MPOA (t (18) = 3.44, P

Interesting about dopamine I thought different.

Very interesting article about dopamine and the affects drugs and other activities have on it. I also thought that people taking the drugs had increased levels of dopamine increasing pleasure and their experience which would be the main reason for addiction. A friend of mine was taking oxycotton, as well as being dependent on other pharmaceuticals. He tried an in him treatment program where he couldn't contact anyone other then family for a couple of weeks but it didn't work out so he's gone to narconon and is getting some great drug treatment now.

As I understand it

dopamine, although critical to optimism and cheerfulness when at balanced levels, is a problem when it goes too high AND when it drops too low (following those peaks). The highs are definitely an enticement...but most addicts would willingly pass them up...if it weren't for the miserable lows, the withdrawal part of the cycle.

As far as I am concerned

As far as I am concerned dopamine is an addictive drug just like the rest. Addiction can have deep effects on us, effects that can lead us to tragic episodes. I think this article is perfect for the informations it provides for us, making us aware of everything we should know for our safety. I was addicted to morphine, and put me to the ground, I couldn't make my own decisions anymore. it was a tough fight but I have my life back.

Dopamine isn't a drug, it's

Dopamine isn't a drug, it's a neurotransmitter. Drugs affect the reward system, of which Dopamine is a part. WHen you take a drug, it's chemical effect is to overload your mind with dopamine. It's essentially a short-circuiting of the process.