News from the frontiers of brain science the brain-glue glia is useful.
Since just the majority of the cells in your brain is glia cells there might be somewhat useful information to know that the glia is not just about gluing the brain together, glia actually has a very important function to. But the fact that glia has been neglected for so many years are very impressive and might also tell us something about how fantastic selective.
If senses make sense then glia makes sense, since animals without glia lose their senses…
Neglected for centuries it might come as a stroke of lightening that 85% of the cells in your brain actually have a major function besides gluing the chemical synapses together, isn’t it fantastic? But the fact that glial cells have been largely neglected the last 100 years speaks with a very interesting voice about how selective and possibly even dysregulated the science of today can be. 2010 did the journal Science a special section on glia and the cells that is
Links about increasing the function of glia and what can happens when a low function increases with the glial growth stimulation factor. Science and Nuts at netvibes.
Can brain grow up and heal from a destructive addiction to narcotic drugs? Yes, probably, some ways seems hopeful but yet dangerous. Ibogaine up-regulates the feedbackloop of GDNF (Glia Derived Neurotrophic Factor) in the brain and it stays up-regulated for at least some months and this seems to be the mechanisms of the antiaddictive effects of Ibogaine. But Ibogaine is also associated with some fatalities when taken in a non-medical setting.
David Graham Scott has been addicted to drugs for nearly 20 years, or as he puts it, “four on heroin and the rest on methadone.” You will stay alive but can you really feel the life? David decides to try the potentially dangerous substance Ibogaine.
Filmed by Scott himself over a five-year period, this emotionally charged documentary follows his double life as a heroin abuser and filmmaker, his pattern of deceit with his family, his battle to conquer methadone, and the fight to finally beat his addiction. His desperation to overcome drugs causes him to risk all on an unauthorized, controversial, and potentially lethal method that promises to limit withdrawal symptoms to one day—but sends the patient on a soul-searching, gut-wrenching 36-hour detox. Some content may be objectionable, and some language may be offensive. But not more offensive than the reality it comes from.
Broadcast by BBC 2004 (One Life). Gold Medal winner New York Film Festivals 2005.
Dr. Deborah Mash speaks about ibogaine and addiction. A short Clip from: BBC’s Horizon Special Psychedelic Experience. Dr Deborah Mash comments Voices from the underground about a mystic substance that is supposed to have more or less magic effects on hardcore addicts. Is it true or just another nut from the crackheads? You tell me.
-Look how dark the world becomes when i close my eyes!
An effective treatment can always be dangerous. A knife can kill, but also cut bread. But really? The knife probably don’t do it by itself?
This will tell us that less than 20 persons have died in after taking ibogaine, the last 50 years. And that an powerful substance like ibogaine should be taken in an clinical setting. So rather than claim that ibogaine is dangerous without telling why, some authorities really makes ibogaine more dangerous than it have to be, by making it illegal.
Gasolin can cause more hallucination, it is cheaper, easier to get and culd be really fun according to some inhalers. Ibogaine is not fun, not addictive – but it can cure addiction, do we know something like this?
On behalf of what authority can anyone say that ibogaine is dangerous without declaring what they are comparing with. Let us look at Methadone, is Methadone a safe drug?
And the fact that the best way to ensure the most dangerous ibogaine effects is to keep ibogaine illegal so that the desperate addicts don’t have a choice.
Let’s look at the alternatives on the market are they just non dangerous substances that induces society with happy people that love everyone else? And want to bless the fact that we have methadone?
Pain pills are the new “pocket gold” on the street, so valuable to drug dealers that the neighborhood prescription counter has become the target of routine holdups.
Pain pills are the new “pocket gold” on the street, so valuable to drug dealers that the neighborhood prescription counter has become the target of routine holdups. Terry and Lisa Houston lost their 17 year old son, Michael. The autospsy report showed he had the equivalent of one tablet of methadone in his system.
No matter how it is acquired, illegally or by prescription, methadone is now the leading drug killer in many states. In North Carolina, methadone-related deaths have increased by 50 times in recent years, skyrocketing to more than one death every other day.
Boosting Brain Protein Quickly Cut Excessive Drinking. If you like to compare ibogaine with Methadone please get the facts right. Beside that, ibogaine tends to make people less proned to take drugs, Methadone don’t work in that way.
So if ibogaine is just to dangerous, what are you really comparing with? I think that the most dangerous thing here is to not get the facts straight. What do you think?
The question about the long term effectiveness of ibogaine remains to be answered and so is the consequences of offering methadone instead of ibogaine.
The name of the blog is inspired by two neurotrophic factors. The first one: GDNF or Glial cell-derived neurotrophic factor is a neurotrophic factor that play key roles in the control of growth and differentiation of the dopamin neuron, and as an potent survival factor for dopaminergic, noradrenergic and spinal motor neurons. In Parkinson’s disease the results have been mixed, but some results are fantastic.
GDNF and the Amgen trial.
Anti-Addicive effect of GDNF
The antiaddictive effects of Ibogaine is mediated by GDNF in the ventral tegmental area. Researchers found that GDNF infusion very rapidly and dose-dependently reduced rat ethanol, self-administration:
Importantly, we demonstrate that GDNF infused into the VTA alters rats’ responses in a model of relapse. Specifically, GDNF application blocked reacquisition of ethanol self-administration after extinction. Together, these results suggest that GDNF, via activation of the MAPK pathway, is a is a fast-acting selective agent to reduce the motivation to consume and seek alcohol. fast-acting selective agent to reduce the motivation to consume and seek alcohol. (1)
we showed that the sustaineda ctions of ibogaine are mediated via an autoregulatory positive feedback loop in which GDNF triggers its own expression.
Ibogaine have been used to cure addictions from:Heroin, Morphine, Methadone and Painkillers.
Could the answer to America’s drug problem lie in an African root? Supporters say Ibogaine can treat Oxycontin, Vicodin, alcohol and heroin addiction.
(1) GDNF is a fast-acting potent inhibitor of alcohol
consumption and relapse
Sebastien Carnicella, Viktor Kharazia, Jerome Jeanblanc, Patricia H. Janak, and Dorit Ron
The Ernest Gallo Research Center and †Department of Neurology, University of California at San Francisco, Emeryville, CA 94608
Edited by Hans Thoenen, Max Planck Institute of Neurobiology, Martinsried.
Why and how ibogaine modulates the desire to consume alcohol in rats: Alcohol addiction manifests as uncontrolled drinking despite negative consequences. Few medications are available to treat the disorder. Anecdotal reports suggest that ibogaine, a natural alkaloid, reverses behaviors associated with addiction including alcoholism; however, because of side effects, ibogaine is not used clinically. In this study, we first characterized the actions of ibogaine on ethanol selfadministration in rodents. Ibogaine decreased ethanol intake by rats in two-bottle choice and operant self-administration paradigms.
Ibogaine also reduced operant self-administration of ethanol in a relapse model. Next, we identified a molecular mechanism that mediates the desirable activities of ibogaine on ethanol intake. Microinjection of ibogaine into the ventral tegmental area (VTA), but not the substantia nigra, reduced self-administration of ethanol, and systemic administration of ibogaine increased the expression of glial cell line-derived neurotrophic factor (GDNF) in a midbrain region that includes the VTA. In dopaminergic neuron-like SHSY5Y cells, ibogaine treatment upregulated the GDNF pathway as indicated by increases in phosphorylation of the GDNF receptor, Ret, and the downstream kinase, ERK1 (extracellular signal-regulated kinase 1). Finally, the ibogaine mediated decrease in ethanol selfadministration was mimicked by intra-VTA microinjection of GDNF and was reduced by intra-VTA delivery of anti-GDNF neutralizing antibodies. Together, these results suggest thatGDNFin theVTAmediates the action of ibogaine on ethanol consumption. These findings highlight the importance of GDNF as a new target for drug development for alcoholism that may mimic the effect of ibogaine against alcohol consumption but avoid the negative side effects.
The up-regulation of GDNF
Human reports and studies in rodents have shown that a single administration of Ibogaine results in a long-lasting reduction of drug craving (humans) and drug and alcohol intake (rodents).
Here we determine whether, and how, Ibogaine exerts its long-lasting actions on GDNF expression and signaling. Using the dopaminergic-like SHSY5Y cell line as a culture model, we observed that short-term Ibogaine exposure results in a sustained increase in GDNF expression that is mediated via the induction of a long-lasting autoregulatory cycle by which GDNF positively regulates its own expression. We show that the initial exposure of cells to Ibogaine or GDNF results in an increase in GDNF mRNA, leading to protein expression and to the corresponding activation of the GDNF signaling pathway. This, in turn, leads to a further increase in the mRNA level of the growth factor. The identification of a GDNF-mediated, autoregulatory long-lasting feedback loop could have important implications for GDNF’s potential value as a treatment for addiction and neurodegenerative diseases.—He, D.-Y., Ron, D. Autoregulation of glial cell line-derived neurotrophic factor expression: implications for the longlasting
actions of the anti-addiction drug, Ibogaine. More here
Maybe impressions from drugs and persons with visions have created al religions as we know them, have inspired countless artworks, musical escapades smash hits and countless tragic deaths. So to deny the importance of drugs in society seems to just create a state of denial.
But as drugs can inspire and sometimes help, we also have to realize something we can’t see, the dead ones and the addicts who take their last breath in this very moments. Those who standing beside the 99-years old woman who says -i have been smoking cigarettes al my life and drinking whiskey to. But how often can we really see the choir of persons standing beside them without any body at al? How often do we listen to the message from the true witnesses? They paid al they had and now they don’t even have a voice, shall we really listen to them?
The science of Antiaddiction
With that in mind, we could realize that drugs have it’s ups and downs and that there is an shure hell getting caught in severe addiction. Here you can find more scientific information about ibogaine.
Could the answer to America’s drug problem lie in an African root? Supporters say Ibogaine can treat Oxycontin, Vicodin, alcohol and heroin addiction. Some former drug addicts swear by it. Others warn it’s too dangerous. In this Special Assignment investigation, CBS 2’s Laura Diaz explores the “Root Of Hope”.
CAC News on Ibogaine Treatment 20 Feb, 2004 – BAY AREA (KRON 4) – Drug addiction has been the plague of modern America. But that could now change forever. What started as a rumor may now actually be an incredible breakthrough in the battle against addictions.
GDNF Mediates the Desirable Actions of the Anti-Addiction Drug Ibogaine against Alcohol Consumption
Ibogaine-GDNF & related at Scribd.
In this study, they first characterized the actions of ibogaine on ethanol self-administration in rodents. Ibogaine decreased ethanol intake by rats in 2 bottle choice and operant self-administration paradigms. Ibogaine also reduced operant self administration of ethanol in a relapse model. Next, they identified a molecular mechanism that mediates the desirable activities of ibogaine on ethanol intake.
BIG News in Alcohol Addiction: New Findings on Growth
Factor Pathways BDNF, Insulin, and GDNF
In recent years, it has become clear that growth factors are not only critical for the development of the central nervous system (CNS) but may also be important contributors to other neuronal functions in the adult brain.
A decrease in the function of a particular growth factor increases the behavioral effect of alcohol. Increases in GDNF and BDNF are reported to decrease alcohol intake, whereas decreases in BDNF are associated with increased alcohol intake. In addition, decreases in insulin signaling lead to increases in the intoxicating effects of alcohol. Hence, these 3 factors may be important nervous system defenses against pharmacological effects of alcohol on behavior.
Data accrue on “visionary” agent to interrupt addiction. Few therapies exist for drug addiction, and unfortunately one agent that has shown promise– the plant alkaloid ibogaine–is mostly given in unsafe settings by addict self-help groups, says Deborah Mash (University of Miami, FL, USA). This means there is a “poverty of clinical data” on the effects of the preparation. However, Mash now has preliminary findings from almost 100 patients, and at a series of talks in the UK this month, she presented her results and called for further research to be top priority.
Ibogaine’s anti-addictive properties have been shown in animals; in human beings, ibogaine often causes “dream-like states” at treatment doses but is quickly cleared from the bloodstream. The persistent metabolite noribogaine should act to raise mood, ward off craving, and help an addict enter long-term therapy via its actions on both the serotonin transporter and on opiate receptors µ and kappa (see Lancet 1998; 352: 1298).
After a single treatment, Mash’s team found that Beck Depression Inventory scores improved significantly (mean 18 vs 4), and remained low for at least a month. There were also significant decreases in craving scores and in physician-rated signs of opiate withdrawal. Adverse events seen during the acute treatment phase were nausea, vomiting, mild tremors, and transient ataxia; initial drops in heart rate and blood pressure occurred in a few patients, mainly “crack” cocaine abusers. “Whether the visions are important [for efficacy], I cannot yet say”, notes Mash, “but there are very profound experiences associated with ibogaine that can be life-transforming”.
Despite these promising results, further drug development is likely to be hindered by continuing controversies. Ongoing litigation over patent rights between the University of Miami and Howard Lotsof, the discoverer of ibogaine’s anti-addictive effects, seems likely to deter potential investors. In addition, some experts have reported cerebellar Purkinje-cell loss in rats treated with high doses of ibogaine. However, Mash found no such damage at necropsy of one former patient who died from other causes. Finally, proponents of ibogaine believe that clinical use of a US schedule-I drug is politically unpalatable in the USA, despite evidence of the lack of abuse potential.
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