6 replies to this topic

[axonopathy]

"Modafinil is a widely-prescribed wakefulness promoting agent that is generally safe and well-tolerated at prescribed dosages. However, the theoretical possibility of tipping the balance toward excitotoxicity exists, since modafinil enhances extracellular glutamate release in hypothalamic regions [9] with concomitant decrements in gamma-amino-butyric acid (the most ubiquitous inhibitory neurotransmitter in the CNS). This two-pronged effect whereby excitatory signaling is enhanced and gabaeric signaling is suppressed raises questions about the potential neurotoxicity of modafinil in combination with other allosteric modulators of glutamate receptors, such as the racetams."

 

Is there a consensus on this issue? Is this fear overblown given that the glutamate/gaba ratio increase seems mostly restricted to hypothalamic brain regions? 

 

 

 

 

Edited by YOLF, 15 May 2015 - 04:33 AM.
link removed

[dancarlin0]

Rnapolymermase is astroturfing for BlueBrainBoost/BrainProTips. Buy a thread bro.

[axonopathy]

Rnapolymermase is astroturfing for BlueBrainBoost/BrainProTips. Buy a thread bro.

 

I actually had to look up astroturfing. Great term.  [link removed] is my website, I'm super proud of it. 

 

I'll keep the blogspam to a minimum from now on. I just got booted out of school so now I have nothing better to do than spam forums about nootropics and stare at the radiator. 

Edited by YOLF, 15 May 2015 - 04:34 AM.

[dancarlin0]

 

Rnapolymermase is astroturfing for BlueBrainBoost/BrainProTips. Buy a thread bro.

 

I actually had to look up astroturfing. Great term. [link removed] is my website, I'm super proud of it. 

 

I'll keep the blogspam to a minimum from now on. I just got booted out of school so now I have nothing better to do than spam forums about nootropics and stare at the radiator. 

 

 

Your writing is really good and well thoughtout. But I would just say be more open with your connections so you can gain people's trust. I mean D-serine and pure methylene blue are good additions to the community. But speaking for myself I'm less likely to buy something if I feel the guy wasn't completely honest. These chemicals would be going into my body, so I need to know the guy isn't a jabroni.

Edited by YOLF, 15 May 2015 - 04:35 AM.

[YOLF]

Sorry to hear you got kicked out. What happened?

 

If your blog is legit, you're welcome to use our XML-RPC interface. Then you can actually support us by blogging on our site and not spamming. You're free to advertise in your blog, but advertising Modafinil would be a grey area as it's RX only in the US, definitely can't advocate for illegal ordering.

 

 

[axonopathy]

Sorry to hear you got kicked out. What happened?

 

If your blog is legit, you're welcome to use our XML-RPC interface. Then you can actually support us by blogging on our site and not spamming. You're free to advertise in your blog, but advertising Modafinil would be a grey area as it's RX only in the US, definitely can't advocate for illegal ordering.

 

I'd love to support the longecity community - I've been browsing this forum for years. How do I apply to write blog posts?

 

Don't worry, I am not a modafinil vendor nor do I wish to promote modafinil sales in any way, so there won't be any legality issue. 

 

Thanks for not banning me and take care. 

[OneScrewLoose]

I would not worry about it at all. The primary mechanism of modafinil is its function as an orexin agonist. Everything else is secondary (not to say irrelavant). Take a look at these:

Modafinil attenuates meth-induced excitotoxicity.

Even more interesting is this study.

Previous reports have shown that modafinil can increase extrasynaptic glutamate in other brain areas (Ferraro et al., 1997; Ferraro et al., 1998; Ferraro et al., 1999). Here, we found increases in nucleus accumbens glutamate in cocaine-experienced, but not naïve animals. This argues that cocaine-induced adaptations interact with modafinil effects on accumbens glutamate. Chronic cocaine down-regulates cystine-glutamate exchange as well as glial glutamate transport via GLT-1 in the accumbens, and this glutamate dysregulation has been strongly linked to reinstatement of cocaine seeking (Kalivas, 2009). Down-regulated GLT-1 mediates the increase in glutamate over-flow measured by microdialysis in the accumbens during cocaine-induced reinstatement (Knackstedt et al., 2010), so it seems probable that down-regulated GLT-1 also contributes to the augmented increases in glutamate by acute modafinil in cocaine-experienced rats.

Even if modafinil does significantly increase glutaminergic activity in those without addiction, that is synonymous with excitotoxicity. Excitotoxicity is an extreme of glutamine release, otherwise the racetams would excitotoxic.