I'll kick it off with this one, do look it up on the pubmed, you can get the entire article for free :
J Neurophysiol. 2000 Jun;83(6):3299-309. Related Articles, Links
Anabolic steroids induce region- and subunit-specific rapid modulation of GABA(A) receptor-mediated currents in the rat forebrain.
Jorge-Rivera JC, McIntyre KL, Henderson LP.
Department of Physiology, Dartmouth Medical School, Hanover, New Hampshire 03755, USA.
Anabolic-androgenic steroids (AAS) have become significant drugs of abuse in recent years with the highest increase reported in adolescent girls. In spite of the increased use of AAS, the CNS effects of these steroids are poorly understood. We report that in prepubertal female rats, three commonly abused AAS, 17alpha-methyltestosterone,Stanozolol, and nandrolone, induced rapid and reversible modulation of GABAergic currents in neurons of two brain regions known to be critical for the expression of reproductive behaviors: the ventromedial nucleus of the hypothalamus (VMN) and the medial preoptic area (mPOA). All three AAS significantly enhanced peak synaptic current amplitudes and prolonged synaptic current decays in neurons of the VMN. Conversely all three AAS significantly diminished peak current amplitudes of synaptic currents from neurons of the mPOA. The endogenous neuroactive steroids, 3alpha-hydroxy-5alpha-pregnan-20-one and 5alpha-androstane-3alpha,17beta-diol, potentiated currents in the VMN as did the AAS. In contrast to the negative modulation induced by AAS in the mPOA, the endogenous steroids potentiated responses in this region. To determine the concentration response relationships, modulation by the AAS, 17alpha-methylTestosterone(17alpha-meT), was assessed for currents evoked by ultrafast perfusion of brief pulses of GABA to acutely isolated neurons. Half-maximal effects on currents elicited by 1 mM GABA were elicited by submicromolar concentrations of AAS for neurons from both brain regions. In addition, the efficacy of 10(-5) to 10(-2) M GABA was significantly increased by 1 microM 17alpha-meT. Previous studies have demonstrated a striking dichotomy in receptor composition between the VMN and the mPOA with regard to gamma subunit expression. To determine if the preferential expression of gamma(2) subunit-containing receptors in the VMN and of gamma(1) subunit-containing receptors in the mPOA could account for the region-specific effects of AAS in the two regions, responses elicited by ultrafast perfusion of GABA to human embryonic kidney 293 cells transfected with alpha(2), beta(3), and gamma(2) or alpha(2), beta(3), and gamma(1) subunit cDNAs were analyzed. As with native VMN neurons, positive modulation of GABA responses was elicited for alpha(2)beta(3)gamma(2) recombinant receptors, while negative modulation was induced at alpha(2)beta(3)gamma(1) receptors as in the mPOA. Our data demonstrate that AAS in doses believed to occur in steroid abusers can induce significant modulation of GABAergic transmission in brain regions essential for neuroendocrine function. In addition, the effects of these steroids can vary significantly between brain regions in a manner that appears to depend on the subunit composition of GABA(A) receptors expressed.
Good things come to those who weight.
The Big Cat is a researcher and theoreticist. His advice must never be taken in the stead of proper advice from a medical professional, it is entirely intended for research purposes.
One thing i did find interesting is that part where in contrast to neuroactive steroids, AAS had negative modulation. THese neuroactive steroids include the 5-Alpha reduced version of progesterone and 5AA. This would definitely mean serious implications for the users of 5AR blockers, or people who choose not to use testosterone as a base.
Good things come to those who weight.
The Big Cat is a researcher and theoreticist. His advice must never be taken in the stead of proper advice from a medical professional, it is entirely intended for research purposes.
Very interesting study BC!
Been running a search and came up with this intially which I have to look up in the library tommorow since it shows that ''These data demonstrate that the effects of AAS exposure on GABAA receptor expression are superimposed upon dynamic developmental changes that accompany the transition from puberty to adulthood''
Anabolic androgenic steroids induce age-, sex-, and dose-dependent changes in GABAA receptor subunit mRNAs in the mouse forebrain
K. L. McIntyrea, D. M. Porterb and L. P. Henderson
peace
j
Just happens to be what I am thinking about including for my studies as a grad(when I get my assoc, and then B.A. of course)...
I have a few studies showing the possibility that a few test AAS had an effect that caused increase of metabolism of monoamines like 5-HT & NE...If I can find the study I'll post it.
One theory that I have been pondering is the effects of Testosterone on the Left side of the brain. I am reading a book on neuroscience at the moment and it talks about the development/mechanics of the mind. And in boys, at puberty, the increase in testosterone had an effect on the size of the left side of the brain. This side of the brain being closely assoc'd with logic, the larger size meant that the brain had more of an ability to process data(and at faster speeds). Now wether or not this effects the standard adult(because although they say the developmental stages really cut off somewheres around the age of 12, there is a possibility that it still might. If cycles of testosterone do have an effect on the size of this portion of the mind. It could mean that testosterone could play a large role in the treatment of alzheimers.....Ahh, still dreaming actually doing research someday...
There also is the data showing decreased aggression from DHEA showing a positive modulation of GABA receptors, but also might signal a positive modulation of 5-HT receptors.
I will say this, while using a combo of tren/prop/winny, my tolerance for GABA has increased...before 500mg would give me the nerve tingles/short of breath.....at about week 4 of 6 I noticed that I could tolerate 1 gram....it isn't taken ED, sometimes not all, so it might signal a greater need for external source....like the niacin flush...someone once told me that the reason there is a niacin flush is because the body had become saturated with niacin(now I am not to familiar with the process, but if it does then would the same hold true for a neurotransmitter? GABA flush because alot isn't needed, no GABA flush more is needed(and accepted))......
These are most just ponderings, and I am not sure how close to accurate they are......so correct me if I am wrong
Dropped the masters goal and math, accelrating program - going for the gold D.Sc or Ph.D
.... Performed my first surgery, patient survived, it was a great rush.
I dont feel like going on a pubmed search tonight, heres some random ramblings.
Test-makes me feel great, I am clinically depressed, it works much better than any SSRI I have been prescribed. Sleep quality is much better.
Tren-makes me slightly cocky, eod injects make me a little moody, ed injects seem to keep my mood stable. I fall asleep fine, but wake up a couple times from either night sweats or to urinate, both uncommon occurences for me.
Dbol-despite the supposed dopamine interactions I generally feel like shit on it. Although I dont need as much adderall, makes me able to function and concentrate well on half the normal dosage. I have a hard time falling asleep when on dbol.
Anadrol-I am the exception to the rule, I feel great, almost as good as with Test. No change in sleep.
M 1T-makes me very irritable, I had to up my lexapro dose a bit just to function day to day. Makes me very lethargic and sleepy during the day. I had trouble falling asleep, and had the same symptoms of tren once asleep, night sweats and frequent urination.
Re: I have a load of interest in this field
Just happens to be what I am thinking about including for my studies as a grad(when I get my assoc, and then B.A. of course)...I have a few studies showing the possibility that a few test AAS had an effect that caused increase of metabolism of monoamines like 5-HT & NE...If I can find the study I'll post it.
I think I have it, I have a shitload of studies on the neural effects of steroids. I'm really interested in kicking this around for a while with regards to what possible effects or complications this might have. I must admit that its been a while since I took neurology.
Good things come to those who weight.
The Big Cat is a researcher and theoreticist. His advice must never be taken in the stead of proper advice from a medical professional, it is entirely intended for research purposes.
I dont feel like going on a pubmed search tonight, heres some random ramblings.
No need to stress yourself, we are all old and ugly enough to look the studies up on pubmed So feel free to throw stuff out there you may have read in the past.
Good things come to those who weight.
The Big Cat is a researcher and theoreticist. His advice must never be taken in the stead of proper advice from a medical professional, it is entirely intended for research purposes.
Heres and old thread by Jguns
Testosterone and Cognitive function
19 July 2001
Testosterone improves cognitive function in older men
Short-term supplementation with testosterone could enhance cognitive function in healthy older men, researchers report in Neurology.
Monique Cherrier (University of Washington Medical School, Seattle) and colleagues randomly assigned 25 healthy men, aged 50 to 80 years, to receive a six-week course of weekly testosterone (100 mg) injections or placebo. Cognitive evaluations were conducted at baseline, week three, and week six, and were based on scores from a battery of neuropsychologic tests.
Among the participants receiving testosterone, levels of circulating testosterone increased by an average of 130% by week three and by 116% by week six. Nevertheless, the researchers note that because of aromatization of testosterone, levels of estradiol also increased by an average of 77% at week three and by 73% at week six.
Cherrier's team found that spatial ability and verbal memory were significantly improved among the testosterone group, compared with their baseline cognitive ability and that of the placebo group. However, they point out: 'Improvements were not evident for all cognitive domains, such as selective attention or language, suggesting that increases in serum testosterone or estradiol have selective or specific effects on memory and spatial abilities.'
The authors concede that their results do not explain whether the improvements in cognition are attributable to increased testosterone or estradiol levels, or both. They add that further studies are needed to examine the relative contribution of testosterone compared with estradiol on cognition in men.
Neurology 2001; 57: 80�88
Performance in spatial tasks sensitive to hormonal fluctuations
Women appear to perform better in spatial tasks during the menstrual phase of their cycle compared with the midluteal phase and German scientists believe that hormonal fluctuations are the reason why.
A group led by Dr Markus Hausmann (Ruhr-Universitat Bochum, Germany) studied eight women in their 20s and 30s. The women took part in 3 different tests of spatial abilities on the 2nd and 22nd days of their menstrual cycles. The researchers also took blood samples every three days in order to analyze concentrations of estradiol, progesterone, testosterone, lutenizing hormone, and follicle-stimulating hormone. For two of the tests, the women's scores did not differ significantly for day two and twenty-two. However, scores for the Mental Rotation Test � where they were asked to recognize rotated versions of a figure � were higher for day two of the cycle in all except one of the women. Dr Hausmann also noted that hormonal fluctuations indicated that estrogen and progesterone were related to the women's spatial scores; higher levels of estrogen were linked to lower scores, while higher concentrations of testosterone were linked to higher scores. The group commented that their findings could explain some of the differences between the way men think compared with women. The authors conclude that 'spatial performance is sensitive to hormonal fluctuations over the menstrual cycle and that different aspects of spatial abilities are related to different hormones or hormone combinations'.
No journal research yet, but from the dots I do connect .
The hippocampus is very rich in glucocorticoid receptors, and in cases of depression(or excessive cortisolism) it shrinks. Is it possible that Testosterone as an antidepressant would upregulate the receptors for serotonin on one point, and allow for the hippocampus to return to normal function? Thereby reducing symptoms of depression such as: lack of concentration, inability to focus, and memmory?
I love this, I really think this is what I want to do now for my graduate work...it is just so damn cool!
Dropped the masters goal and math, accelrating program - going for the gold D.Sc or Ph.D
.... Performed my first surgery, patient survived, it was a great rush.
Good point, factor in that testosterone antagonizes those GR's and you may be on to something.
Good things come to those who weight.
The Big Cat is a researcher and theoreticist. His advice must never be taken in the stead of proper advice from a medical professional, it is entirely intended for research purposes.
if that were true there would be a lot of happy focused bbrs running around with eidetic memories.
jb
As always, it's difficult to extrapolate results of tests on the infirmed and apply those to healthy individuals. However this study seems particularly interesting because the pathways through which test allegedly helps spatial coordination could be similarly enhanced in healthy subjects as they were in Alzheimer�s patients. From my brief understanding of the issue (and I mean brief) enhanced acetylcholine release would improve coordination even in subjects who were not deficient.
On a side note...I noticed that I got much better at juggling (a relaxing hobby of mine) during my last brief cycle.
A pilot study on the effects of testosterone in hypogonadal aging male patients with Alzheimer's disease.
Tan RS, Pu SJ.
Geriatric Medicine and Gerontology Programs, Department of Family and Community Medicine, University of Texas, Houston, USA.
The male aging process brings about declines in hormonal function including a gradual decline in bioavailable testosterone levels. Animal studies suggest that testosterone modulates cognitive function through enhancing acetylcholine release and up-modulation of nicotinic receptors. Tau protein deposition is also affected by androgen supplementation in animals. We hypothesize that testosterone replacement in elderly hypogonadal males may improve cognition, in particular the visual-spatial domain. Thirty-six male patients with a new diagnosis of Alzheimer's disease had their total and bioavailable testosterone levels measured. None of the patients had been on acetylcholinesterase inhibitors. Ten of the 36 patients (28%) were deemed biochemically hypogonadal (total testosterone < 240 ng/dl or 7 nmol/l). Five of the hypogonadal patients were randomized to testosterone and five to placebo. Initial Alzheimer's Disease Assessment Scale cognitive subscale (ADAScog) and Mini Mental Status Examination (MMSE) ranged from 31 to 19 and from 17 to 22, respectively. The clock drawing test (CDT) and the pentagon-tracing portion of the MMSE were used as measures of visual-spatial abilities. Normal prostate-specific antigen (PSA) levels were essential before treatment with intramuscular testosterone, 200 mg every 2 weeks. Measurement of testosterone, complete blood count, lipids, PSA and neuropsychological cognitive tests were repeated at 3, 6, 9 and 12 months of treatment. In the testosterone-treated group, levels of total testosterone increased from a mean of 126.4 ng/dl to 341 ng/dl or 3.6 nmol/l to 9.7 nmol/l (p = 0.11). Bioavailable testosterone also increased from a mean of 48.7 ng/dl to 142 ng/dl or 1.39 nmol/l to 4.05 nmol/l (p = 0.10). PSA levels were also elevated from a mean of 0.98 to 1.37 ng/ml (p = 0.07). ADAScog improved from a mean of 25 to 16.3 (p = 0.02); MMSE improved from a mean of 19.4 to 23.2 (p = 0.02), CDT also improved from 2.2 to 3.2 (p = 0.07). One patient stopped treatment because of hypersexual behavior. The placebo-treated group deteriorated gradually. This small pilot study performed in aging male patients suggests that testosterone could indeed improve cognition, including visual-spatial skills in mild to moderate Alzheimer's disease.
It is quite fascinating, and now I have to see if I can find a study on the effects of Test on the hippocampus.
I am thinking that if we could stimulate brain function with test, restoring size to the hippocampus, and perhaps increasing mass of the left side of the brain. It is still going to require mental challenges, perhaps combining testosterone with continuing education. There are a few studies noted in the book I am reading right now (inside the brain) where they tested the IQ's of individuals that went through highschool(stopped), college BA(stopped), Grad(MA, PH.D - then stopped), and those in continuous education. They found that maintainance of intelligence was optimal in those that continually challenged their minds. Meanwhile each step in education resulted in a great percentage of retainment over those that stopped at the lower levels of education.
Dropped the masters goal and math, accelrating program - going for the gold D.Sc or Ph.D
.... Performed my first surgery, patient survived, it was a great rush.
stumbled across this study on Nandrolone
quote:
Med Sci Sports Exerc. 2003 Jan;35(1):32-8. Related Articles, Links
Nandrolone decanoate enhances hypothalamic biogenic amines in rats.
Tamaki T, Shiraishi T, Takeda H, Matsumiya T, Roy RR, Edgerton VR.
Department of Physiology, Uinversity of California, Los Angeles, CA, USA.
PURPOSE: To identify possible mechanisms for an anabolic-androgenic steroid induced increase in aggressive behavior and work capacity, the levels of some biogenic amines considered to be closely related to a systemic hyper-adrenergic state were measured in selected regions of the brain. METHODS: Wistar male rats were divided randomly into five groups: nontreated (control), oil-vehicle-treated (vehicle) or one of three (therapeutic dose and 10- or 100-fold higher dose) anabolic-androgenic steroid-treated (steroid-1, -2, -3) groups. Rats in the steroid and vehicle groups were given a single dose of nandrolone decanoate or oil vehicle, respectively, one week before tissue sampling. The levels of norepinephrine (NE) and its metabolite, 4-hydroxy-3-methoxyphenylglycol (MHPG), serotonin (5-HT) and its metabolite, 5-hydroxy-indole-3-acetic acid (5-HIAA) were measured in the cerebral cortex, hypothalamus and cerebellum by high-performance liquid chromatography. Immunostaining for c-fos was performed as a confirmation of increased neural activity. RESULTS: The levels of NE and MHPG were increased by approximately 2- and approximately 7-fold in the hypothalamus of the steroid-2 compared with the control and vehicle groups. The levels of 5-HT and 5-HIAA were approximately 40 and approximately 50% higher in the steroid-2 compared with the control and vehicle groups. A significantly higher number of c-fos expressing neurons were observed in the periventricular region of the steroid-2 than the control and vehicle groups, indicating enhanced neuronal activity after nandrolone decanoate treatment. CONCLUSIONS: The present results, combined with previously reported findings of physical performance enhancement after anabolic-androgenic steroid treatment, are consistent with the interpretation that elevated levels of adrenergic and serotonergic amines in the hypothalamus could contribute to aggressive behaviors as well as improved physical performance
There was also a study showing down regulation of 5-HT1b receptors and upregulation in 5-HT2 receptors.
In general 5-HT1b is a key receptor involved with the release and synthesis of serotonin. So downregulation would mean that there would be decreased serotonin production, whereas 5-ht2(all that I could find) is that in patients with major depression 5-HT2 receptor density is increased.
Aggression is closely related to both norepinephrine and serotonin.
Just to give you an idea of excessive highs and lows of either biogenic amine.
high norepinephrine is assoc'd with :
excessive arousal, increased impulsive acts, increased heart rate
low norepinephrine is assoc'd with :
lack of arousal, increased affinity to premeditated violence, thrill-seeking (looking for that stimulation)
High serotonin:
shyness, obsessive compulsions, fearfulness, lack of self confidence, decreased aggression
low serotonin:
depression, suicide, impulsive aggression, alcoholism (which first drink would raise it, subsequent would cause it to go down even further - hence the increased propensity for violence), sexual deviance, explosive rage
I also feel that it is the ratio of NE to 5-HT that plays a role in aggression. Also, the psychological plays a huge role as well.
Dropped the masters goal and math, accelrating program - going for the gold D.Sc or Ph.D
.... Performed my first surgery, patient survived, it was a great rush.
Re: stumbled across this study on Nandrolone
I also feel that it is the ratio of NE to 5-HT that plays a role in aggression. Also, the psychological plays a huge role as well.
Excellent point.
I wonder if there are any psychiatric meds that could tip this ratio in an athletes favor. Most psychiatric meds are permitted to be used by tested athletes.
There are many female olympians who are heavilly medicated to treat an array of illnesses that are belived to be some of the many causes of eating disorders in elite women athletes. (I.E. depression, anxiety, and even narcolepsy).
I wonder if any of these meds could in turn make them better athletes by increasing aggression.
The "eating disorder" excuse always seemed a bit suspect to me.