• N&PD Moderators: Skorpio | thegreenhand

  • Neuroscience & Pharmacology Discussion Welcome Guest
    Posting Rules Bluelight Rules
    Recent Journal Articles Chemistry Mega-Thread
    FREE Chemistry Databases! Self-Education Guide

Ketamine salts solubility

Status
Not open for further replies.
sekio said:
J Clin Psychopharmacol. 2014 Feb 12. [Epub ahead of print]
Methylphenidate Enhances Cognitive Performance in Adults With Poor Baseline Capacities Regardless of Attention-Deficit/Hyperactivity Disorder Diagnosis.
Agay N, Yechiam E, Carmel Z, Levkovitz Y.

More evidence that, maybe, stimulants are just good at making people task-oriented, rather than are a "treatment" for anything? I never really bought into the whole "stimulants effect people with AD(H)D differently"... given that, y'know, people in general experience drugs differently, and set and setting need to be considered. Also, given that stimulants like methylphenidate, amphetamine and the like precede the ADHD explosion, and have been known to enhance cognitive performance (in some contexts) for a long damn time.
Click to expand...

2.7k words written on my dissertation in one day agrees with that. ADHD stimulants are just fucking fantastic cognitive enhancers in any population.
 
Black said:
it didn't reach statistical significance. with a probablility of 95% the risk of developing an adenocarcinoma is somwhere between 75% of the normal risk and 400% of the normal risk.
so it "looks like" there could be a correlation between cannabis and lung cancer risk (especially as there is a monotonic association between those factors), so that larger studies could find something, but this study alone still neither proves or disproves anything.
Click to expand...

Yea that makes sense, I just looked at the 1.73 and 1.74 and didn't pay much attention to the range. It just irks me the way that pro-pot publications use that study to argue Smoking Marijuana Does Not Lead to Lung Cancer, when I think you could more easily argue the opposite from that data.
 
Transl Psychiatry. Jul 2014; 4(7): e411.
Published online Jul 15, 2014. doi: 10.1038/tp.2014.30
PMCID: PMC4119213
The atypical antidepressant and neurorestorative agent tianeptine is a μ-opioid receptor agonist
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4119213
...Herein, we report the characterization of tianeptine as a μ-opioid receptor (MOR) agonist. Using radioligand binding and cell-based functional assays, including bioluminescence resonance energy transfer-based assays for G-protein activation and cAMP accumulation, we identified tianeptine as an efficacious MOR agonist (Ki Human of 383±183 nM and EC50 Human of 194±70 nM and EC50 Mouse of 641±120 nM for G-protein activation). Tianeptine was also a full δ-opioid receptor (DOR) agonist, although with much lower potency (EC50 Human of 37.4±11.2 μM and EC50 Mouse of 14.5±6.6 μM for G-protein activation). In contrast, tianeptine was inactive at the κ-opioid receptor (KOR, both human and rat). On the basis of these pharmacological data, we propose that activation of MOR (or dual activation of MOR and DOR) could be the initial molecular event responsible for triggering many of the known acute and chronic effects of this agent, including its antidepressant and anxiolytic actions.
Click to expand...

May explain why it's abusable. :p
 
sekio said:
Transl Psychiatry. Jul 2014; 4(7): e411.
Published online Jul 15, 2014. doi: 10.1038/tp.2014.30
PMCID: PMC4119213
The atypical antidepressant and neurorestorative agent tianeptine is a μ-opioid receptor agonist
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4119213


May explain why it's abusable. :p
Click to expand...

Wow great find, I always thought the "5-HT reuptake enhancer" mechanism was bullshit, this makes a lot more sense.
 
Did anyone else who attended public school in the US learn that identical twins are slightly telepathic?
 
... said:
Did anyone else who attended public school in the US learn that identical twins are slightly telepathic?
Click to expand...


Ummm no, did you go to school in a creationist state by any chance?


CreationismTexas.jpg
 
I must've just had a crazy Science teacher, or one who liked to fuck with us. There's these twin girls in my grad-school class and I'm gonna ask them about telepathy, to break the ice. I'm pretty sure they'll tell me they read one another's thoughts.

We did learn a lot of fallacious shit in public schools though.
 
Ho-Chi-Minh said:
but it really also has to be a bdnf/neurotrophin enhancer in the hippocampus to be a true ad

is it?
Click to expand...

It wouldn't have been approved if it didn't have clinical antidepressant efficacy, doesn't that efficacy alone make it a "true ad"?
 
Given how tentative the neuroplasticity theory of depression is, I would take behavioral evidence of reduced depressive symptoms over confirmation of changes in BDNF any day.

ebola
 
How do you enhance reuptake of a neurotransmitter? Does it bind allosterically with the transporter in order to pry open its doors (so to speak)?
 
but it really also has to be a bdnf/neurotrophin enhancer in the hippocampus to be a true ad
Click to expand...

Well, no. That's just an effect common to many drugs classed as ADs. One could argue that something like buprenorphine would be an effective antidepressant, and I don't think it does anything to BDNF directly. Tianeptine's close cousin amineptine is a dopamine reuptake inhibitor, too. I'm willing to bet that makes you feel good but probably doesn't exactly encourage neuronal growth.

How do you enhance reuptake of a neurotransmitter? Does it bind allosterically with the transporter in order to pry open its doors (so to speak)?
Click to expand...

It was never clearly established what the mechanism of a SSRE would be, and given that tianeptine is basically the only one that was described as such, I concur that it's pretty much bullshit... there are a few problems with the theory, like tianrptine having no affinity for SERT.

Wiki - Reuptake enhancers said:
Tianeptine has no affinity to the serotonin transporter, neither increases nor decreases extracellular levels of serotonin in cortico-limbic structures of conscious rats, and it didn't show any other long-term effect on the serotonin pathway.[ref]
Click to expand...

Really, people throw the term around as a stand in for "antidepressant, mechanism not otherwise specified".
 
Yet the dopaminergic drug amphetamine increases BDNF in the striatum and has AD properties for some (even after long-term use, mostly in the elderly). Realizing that these two effects may be coincidental, some dopaminergics may have neurotrophic activity.
 
Post a link to a study you find interesting!!!

The study doesn't necessarily have to be recent, although if it is, then that's fine too. After your link, write a brief message explaining why you thought the study was interesting. For example,

www.ncbi.nlm.nih.gov/pubmed/24739011

MDPV induces a greater conditioned place preference than amphetamine.
 
http://www.ncbi.nlm.nih.gov/pubmed/23336047

Chronic SSRI treatment exacerbates serotonin deficiency in humanized Tph2 mutant mice. -- while it targets a specific mutation here, I guess SSRIs could potentially lower 5-HT levels in many individuals. Think there are more studies to this topic.

--

The MDPV thing imo is logically as it does have greater affinity to the DAT than amphetamine, which affects NE a bit more than DA.
 
Anybody here studying pharmacology at university? You guys are so eloquent I'm curious what you're working on.

I'm nervous to say what I'm doing, other than it's a professional degree in the medical sciences. I'm thinking about going for a PhD, but I kind of want to start earning once I graduate.
 
Acute toxicity associated with the recreational use of the novel dissociative psychoactive substance methoxphenidine
K. E. Hofer, C. Degrandi, D. M. Müller, U. Zürrer-Härdi, S. Wahl, C. Rauber-Lüthy, and A. Ceschi

Introduction. Methoxphenidine is a novel dissociative designer drug of the diarylethylamine class which shares structural features with phencyclidine (PCP), and is not at present subject to restrictive regulations. There is very limited information about the acute toxicity profile of methoxphenidine and the only sources are anonymous internet sites and a 1989 patent of the Searle Company. We report a case of analytically confirmed oral methoxphenidine toxicity. Case details. A 53-year-old man was found on the street in a somnolent and confusional state. Observed signs and symptoms such as tachycardia (112 bpm), hypertension (220/125 mmHg), echolalia, confusion, agitation, opisthotonus, nystagmus and amnesia were consistent with phencyclidine-induced adverse effects. Temperature (99.1°F (37.3°C)) and peripheral oxygen saturation while breathing room air (99%) were normal. Laboratory analysis revealed an increase of creatine kinase (max 865 U/L), alanine aminotransferase (72 U/L) and gamma-glutamyl transpeptidase (123 U/L). Methoxphenidine was identified by a liquid chromatography tandem mass spectrometry toxicological screening method using turbulent flow online extraction in plasma and urine samples collected on admission. The clinical course was favourable and signs and symptoms resolved with symptomatic treatment. Conclusion. Based on this case report and users’ web reports, and compatible with the chemical structure, methoxphenidine produces effects similar to those of the arylcyclohexylamines, as PCP.
Click to expand...

Nothing like getting picked up off the street by paramedics while all dissociated out.
 
Status
Not open for further replies.
Top