• N&PD Moderators: Skorpio

testoserone

hormones aren't transmitters. Transmitters are released, bind to the receptor and are then taken back up.

Hormones are neuromodulators, IIRC
 
No, it has a function in the endocrine system, not the nervous system.

Common neurotransmitters:

Monoamines:
Serotonin
Dopamine
(Nor)Epinephrine (aka (nor)adrenaline)

Acetylcholine
GABA
Glutamate ("somewhat")
 
thank you everyone, i had this argument with a student in his 4th year at a niice university & he tried to tell me that testosterone was a neuron tranmitter & i called bs (of course) and ima run sum responses his way.
 
Last I read, the definition was contested.

Like neurotransmitters, testosterone binds to receptors and alters cell function.

To my knowledge, the biggest difference between steroids and neurotransmitters is that the former are released into the bloodstream and reach every cell in the body, while the latter are more localized.
 
Jamshyd said:
Last I read, the definition was contested.

Like neurotransmitters, testosterone binds to receptors and alters cell function.

To my knowledge, the biggest difference between steroids and neurotransmitters is that the former are released into the bloodstream and reach every cell in the body, while the latter are more localized.
Hence they call it the "neuroendorcrine system" at times? Heh.
 
hence why i said not classical by any means, but notably some steroids do have well reported NT activities DHEA affects Sigma receptors, certain pregnanolones affect GABA receptors (allo-), progesterone affects dopaminergic channels, pregnenolone improves memory and concentration, and prevents fatigue via both a GABA antagonist activity and positive allosteric modulation at the NMDA receptor as well as affects on ACh release

they are noted as neuroactive steroids as to their more defined NT-like roles, but indeed other hormones like testosterone not such classified indeed have effect on mood and energy that certainly can be as profound as NT or 'classical" NS...perhaps not as directly but note much of the effects of course of some NTs can also be indirect as well
 
It is a neurotransmitter of sorts (much like estrogen, which is very important to the functioning of the brain). It modulates the activity of other neurotransmitter systems in the brain, sometimes permanently as in the case of permanent changes in aggression after it is administered to humans chronically in high dose.
 
sometimes permanently as in the case of permanent changes in aggression after it is administered to humans chronically in high dose.

uh, no...there is no real evidence for this myth
 
I had read a study that showed this somewhere back but I'm having trouble finding it now.

Here is a rat study, though:
Long-term effects of pubertal anabolic-androgenic steroid exposure on reproductive and aggressive behaviors in male rats.
Farrell SF, McGinnis MY.

Center for Anatomy and Functional Morphology, Mount Sinai School of Medicine, New York, NY 10029, USA.

The current study examined acute and long-term effects of anabolic-androgenic steroid (AAS) exposure during puberty on copulation, vocalizations, scent marking, and intermale aggression, both with and without tail pinch, in intact male rats. Animals received 5 mg/kg of testosterone, nandrolone, stanozolol, or vehicle, beginning at puberty. After 5 weeks, behavior tests were performed while continuing AAS injections. AAS treatment was then discontinued. Behaviors were tested during 3-5 weeks, 9-11 weeks, and 15-17 weeks of withdrawal. During AAS administration, stanozolol males showed significant reductions in all behaviors compared with controls, except aggression with tail pinch. Nandrolone treatment significantly reduced vocalizations and scent marking, and testosterone had no significant effect on behavior. During withdrawal, behaviors in stanozolol males recovered to control levels at variable rates: aggression at 4 weeks; mounts, vocalizations, and scent marking at 9 weeks; and ejaculations at 15 weeks of withdrawal. Stanozolol males showed significantly higher levels of tail pinch-induced aggression during every withdrawal test. Nandrolone-treated males scent-marked at control levels by 9 weeks withdrawal but displayed significantly fewer vocalizations and significantly more tail pinch-induced aggression than controls for the entire study. Testosterone-treated males scent-marked significantly below controls at 3 weeks withdrawal and showed significantly more tail pinch-induced aggression at 5 weeks withdrawal. All three AAS significantly increased tail pinch-induced aggression compared with corresponding nontail pinch tests, even at study endpoint. These results suggest that alterations in androgen-dependent behaviors by pubertal AAS exposure can persist long after drug exposure, and some effects may even be permanent.
http://www.ncbi.nlm.nih.gov/pubmed/15256309

It's fairly well established that testosterone and testosterone like compounds mediate changes in mood in humans acutely with administration (not to mention pretty much all mammals as well).

edit: found it, from this thread: http://www.bluelight.ru/vb/showthread.php?t=324331
"Conclusions Testosterone administration, 600 mg/wk increased ratings of manic symptoms in normal men. "1

"...increased aggression after withdrawal from testosterone, nandrolone, and stanozolol, an effect which persisted..."2

"AAS exposure may not cause violent behaviors, but may increase the likelihood that aggressive acts will result in violence. This may persist."

1. Arch Gen Psychiatry -- Abstract: Effects of Supraphysiologic Doses of Testosterone on Mood and Aggression in Normal Men: A Randomized Controlled Trial, February 2000, Pope et al. 57 (2): 133
2. Anabolic Androgenic Steroids and Aggression: Studies Using Animal Models -- McGINNIS 1036 (1): 399 -- Annals of the New York Academy of Sciences
A good overview of psykosis - MJA: Anabolic steroids and the mind

It's interesting if you look at the pharmaceutical funded studies in humans for things like contraceptives and antidepressants where exogenous testosterone is administered, they find all the same things that the other studies do (fairly strong, statistically significant changes in aggression and manic states) but then downplay them as minor and unimportant side effects.
 
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This made me curious, so I looked as well:

Anabolic-androgenic steroid dependence? Insights from animals and humans.

Anabolic-androgenic steroids (AAS) are drugs of abuse. They are taken in large quantities by athletes and others to increase performance, with negative health consequences. As a result, in 1991 testosterone and related AAS were declared controlled substances. However, the relative abuse and dependence liability of AAS have not been fully characterized. In humans, it is difficult to separate the direct psychoactive effects of AAS from reinforcement due to their systemic anabolic effects. However, using conditioned place preference and self-administration, studies in animals have demonstrated that AAS are reinforcing in a context where athletic performance is irrelevant. Furthermore, AAS share brain sites of action and neurotransmitter systems in common with other drugs of abuse. In particular, recent evidence links AAS with opioids. In humans, AAS abuse is associated with prescription opioid use. In animals, AAS overdose produces symptoms resembling opioid overdose, and AAS modify the activity of the endogenous opioid system.http://www.ncbi.nlm.nih.gov/pubmed/...ez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum

Also:

Are androgens reinforcing? Androgenic-anabolic steroids (AAS) are drugs of abuse. They are taken in large quantities by athletes and others to increase performance, often with negative long-term health consequences. As a result, in 1991, testosterone was declared a controlled substance. Recently, Brower [K.J. Brower, Anabolic steroid abuse and dependence. Curr. Psychiatry Rep. 4 (2002) 377-387.] proposed a two-stage model of AAS dependence. Users initiate steroid use for their anabolic effects on muscle growth. With continued exposure, dependence on the psychoactive effects of AAS develops. However, it is difficult in humans to separate direct psychoactive effects of AAS from the user's psychological dependence on the anabolic effects of AAS. Thus, studies in laboratory animals are useful to explore androgen reinforcement. Testosterone induces a conditioned place preference in rats and mice, and is voluntarily consumed through oral, intravenous, and intracerebroventricular self-administration in hamsters. Active, gonad-intact male and female hamsters will deliver 1 microg/microl testosterone into the lateral ventricles. Indeed, some individuals self-administer testosterone intracerebroventricularly to the point of death. Male rats develop a conditioned place preference to testosterone injections into the nucleus accumbens, an effect blocked by dopamine receptor antagonists. These data suggest that androgen reinforcement is mediated by the brain. Moreover, testosterone appears to act through the mesolimbic dopamine system, a common substrate for drugs of abuse. Nonetheless, androgen reinforcement is not comparable to that of cocaine or heroin. Instead, testosterone resembles other mild reinforcers, such as caffeine, nicotine, or benzodiazepines. The potential for androgen addiction remains to be determined.http://www.ncbi.nlm.nih.gov/pubmed/15488545?ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.Pubmed_Discovery_RA&linkpos=1&log$=relatedarticles&logdbfrom=pubmed

Interesting. Evidently testosterone exhibits some reinforcing properties. From what I understand, certain steroids produce a greater sense of well-being than others, such as methandrostenolone. In contrast, steroids like oxymetholone supposedly do not result in a strong sense of well-being, presumably because it is more estrogenic or because of a higher side-effect profile.

A while back I "accidentally" injected (IM, thankfully) some testosterone thinking it was mexican ketamine (according to my friend it was mixed esters, and I had injected just over 2ml, which is essentially 500mg+ of testosterone). A few days later I started to feel a bit nervous/edgy, and there appeared to be an element of CNS-stimulation. Later on, at around 6-7 days after the injection, the nervousness subsided and I was better able to feel the mood-lift, but nothing too significant. When i briefly took 4-androstenedione capsules in high school I noticed a similar type of CNS-stimulation; it was far faster acting but not as intense/sustained as the injection.

I didn't think it was reinforcing, but then again, I was not injecting it "intracerebroventricularly".
 
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