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substances that stimulate brain cell growth

Actually cannabis stimulates apoptosis, very good for the body, but doesn't help grow new brain cells.
 
stimulating cell growth shouldnt be considered as a good thing. keep in mind that cancer is simply the uncontrollable & unavoidable cell growth. its pointless and dangerous to take drugs to do it. every cell has a limited life time. at some point they need to kill themselves so other cells can reproduce and replace - this is called apoptosis as hammilton mentioned above and imo taking drugs to "stimulate" this process is dangerous and may lead to perma damage
 
Be careful how you phrase your question, as I think everyone thus far has misunderstood you.

I assume you're not talking about mitosis, since you said "grow." You're talking about an actual increase in neuron and/or neural-organelle volume? But of course, neuron volume in this case would not be as important as localized neural density and interconnectivity. A substance that could enhance these traits selectively (with structure-specificity) would be very useful. There are many possible applications, but 2 examples that immediately come to mind are the correlation between phobias and an undersized amygdala, and the cortical and hippocampal shrinkage typical of Alzheimer's-stricken brains. There are so many more examples in which size does indeed matter (if even only at the structural level, as overall human brain size is not directly correlated with intelligence level).
 
Ergoloids (e.g. hydergine, LSD, ergometrine, bromocriptine) are known to stimulate neurogenic processes by promoting the release of the neurotrophic factor BDNF and upregulating transcription of the synaptic plasticity protein arc. Acute LSD has been shown to upregulate transcription of arc mRNA in the rat prefrontal cortex by upwards of three-fold (Nichols and Sanders-Bush, 2002; Nichols et al, 2003). Several ergoloids with dopaminergic agonist activity (bromocriptine, lisuride, LSD) have also been found to upregulate expression of the central anti-apoptotic protein Bcl-2 (Kihara et al, 2002; Caraci et al, 2005).

Then again, these effects are pretty much related solely to synaptogenesis--they would likely increase synaptic plasticity, but not cause a whole bunch of new neurons to just emerge. True uncontrolled neurogenesis is not always a good thing. In addition to the cancer risks mentioned, large-scale neurogenesis is known to occur after massive seizures and status epilepticus. Since those new hippocampal neurons don't necessarily "wire together" in a normal manner, it can lead to greater susceptibility to future seizures as well as cognitive wigginess.
 
thc/cannabinoids has been shown to cause neurogenesis



"Researchers at the University of Saskatchewan in Saskatoon found that the administration of synthetic cannabinoids in rats stimulated the proliferation of newborn neurons (nerve cells) in the hippocampus region of the brain and significantly reduced measures of anxiety and depression-like behavior."



http://norml.org/index.cfm?Group_ID=6812
 
melange said:
thc/cannabinoids has been shown to cause neurogenesis

"Researchers at the University of Saskatchewan in Saskatoon found that the administration of synthetic cannabinoids in rats stimulated the proliferation of newborn neurons (nerve cells) in the hippocampus region of the brain and significantly reduced measures of anxiety and depression-like behavior."

http://norml.org/index.cfm?Group_ID=6812
Click to expand...

I don't think what is true of synthetic cannabinoids is neccessarily true of THC itself, though HU210 is mighty close in structure. I wonder if the mechanism has been elucidated.

Has any study actually shown THC proper to stimulate neurogenesis?
 
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Lots of things stimulate neurogenesis.

Novel situations stimulate neurogenesis.

Learning things stimulates neurogenesis.

Citicoline (CDP-choline) is a great one.

DHEA. Ashwagandha. Fluoxetine. Hydergine.

Amphetamine, dose-dependently, also stimulates neurogenesis. So does methylphenidate.

Sources available upon request.

Cannabis does indeed promote neurogenesis Synthetic cannabinoids, at least, have been shown to promote neurogenesis: http://biopsychiatry.com/cannabinoids-neogenesis.htm

It also does indeed stimulate some apoptotic enzymes, which may be the main source of the apparently recoverable hippocampal damage (a similar thing to the effects of stress, depression, mania, sleep deprivation, etc.) that is seen with heavy use.

In practice, it seems to me that a lot of people who smoke too much pot often stop doing/learning novel things and stop being agents of novelty, though this is not true for everyone.

Hey: citicoline is protective, at least on paper, against induction of said apoptotic enzymes. Though maybe ingesting cholinergics with cannabis (an acetylcholinesterase inhibitor, amongst its gajillion other actions) could be unpleasant for some.
 
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Amphetamine and MPH?

A brief fragment fom a quick and unexhaustive search:


These findings suggest that decreased adult neurogenesis is an enduring consequence of early-life exposure to MPH and are discussed for their relevance to humans

and (from a different article)

....could potentially compromise the function of the dentate gyrus in adults.
Click to expand...

I will cite the references if need be...
 
J Hypertens. 2008 Mar;26(3):544-52.

Candesartan but not ramipril pretreatment improves outcome after stroke and stimulates neurotrophin BNDF/TrkB system in rats.Krikov M, Thone-Reineke C, Müller S, Villringer A, Unger T.
Center for Cardiovascular Research (CCR)/Institute of Pharmacology, Charité-Universitätsmedizin Berlin, Berlin, Germany.

OBJECTIVES: Drugs interfering with the renin-angiotensin system (RAS) have been shown to reduce the incidence of stroke in patients at risk and to afford neuroprotection in experimental brain ischemia. This study aimed to compare potential neuroprotective effects of systemic pretreatment with the angiotensin receptor blocker, candesartan, and the angiotensin-converting enzyme (ACE)-inhibitor, ramipril, in normotensive Wistar rats after focal cerebral ischemia, with special emphasis on the regulation of neurotrophins. METHODS: Equipotent subcutaneous doses of candesartan and ramipril were determined via inhibition of pressor responses to intravenously injected angiotensin II (Ang II) or angiotensin I (Ang I), respectively. Accordingly, animals were treated with candesartan (0.1 mg/kg body weight, twice daily), ramipril (0.01 and 0.1 mg/kg body weight, twice daily) or vehicle (0.9% saline, twice daily), respectively, 5 days prior to middle cerebral artery occlusion (MCAO) with reperfusion. Severity of stroke was estimated via infarct size [magnetic resonance imaging (MRI) 48 h after MCAO] and neurological outcome (24 h, 48 h after MCAO). Measurements of neurotrophins/receptors in brain tissue were performed 48 h after MCAO. RESULTS: Pretreatment with candesartan and ramipril (low dose) did not reduce blood pressure during MCAO, whereas ramipril high dose did. Candesartan, but not ramipril at any dose, significantly reduced stroke volume and improved neurological outcome. Poststroke mRNA and protein of the neurotrophin receptor, TrkB, were significantly elevated in animals treated with candesartan, but not ramipril. CONCLUSIONS: Systemic pretreatment with a sub-hypotensive, RAS-blocking dose of candesartan affords neuroprotection after focal ischemia, associated with increased activity of the neurotrophin BDNF/TrkB system. Ramipril at sub-hypotensive and hypotensive, RAS-blocking doses showed no significant neuroprotective effects.

PMID: 18300867 [PubMed - indexed for MEDLINE]
 
Don't forget that neurogenesis can mean alot of things. Sure, we do have a relatively constant number of braincells throughout life (unless something kills them, ofc).

I heard a 4 hour show and tell from a danish Ph.D scientist in neurology and neuroanatomy. She definately had alot going for her, she is the head of an entire team of researchers and students on their expedition to learn more on braincells and synapse. They study in Copenhagen University btw.

The difference is in the neuron synapsis threads. These connections is how braincells communicate. There are 100.000's of connections - virtually unlimited - to a single one. When you learn new stuff, experience something new or learn to do something - you are experiencing a form of neurogenesis.

You are not creating new/more braincells, only sufficient to replenish the old, dead ones.. No, you are creating new connections. That is why, parkinsons for instance cuts your connections slowly. You don't remember how to ride a bike, don't remember your family and friends - etc.



Interesting article on LSD and the "mind-at-large" #7..
Also, if you haven't already, read the stanislav grof books - they're cool and exiting, interesting books on LSD and the human psycbe.
 
I know GHB has been linked to cell proliferation (Psychopharmacology, Julien). I think it was found to decrease apoptosis.
If you're not only interested in recreational drugs, then the broader class of NDMA agonists may be of interest to you. Try doing a search for cell profileration and hippocampus.
The hippocampus is a good place to look at this to answer this question because its been the site of a lot of research due to its importance in learning and memory.
As someone so appropriately mentioned, cell proliferation is not always a good thing. And no, you never possess ALL the neurons you will ever possess, that is impossible.
Our brains have two major (known) sites where neural stem cells (herein NSC) are generated. These new NSCs then migrate to their respective areas, in the hippocampus, and the olfactory bulb.
 
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