• N&PD Moderators: Skorpio | thegreenhand

⫸STICKY⫷ The N&PD Recent Journal ARTICLE Club


Nov 7, 2004
Nuke again,

This was recommended recently and I think could be a positive addition to ADD.

In this thread we will contribute short summaries of recent articles related to drugs, licit or illicit, such as biochemistry, psychopharmacology or botany. I'd encourage you to simply head to the websites of your favourite journals and browse their indexes or just to search on pubmed about topics that interest you.

I think the following format will lend well to keeping the contents of this thread organized:

1.) Title of work
2.) Authors
3.) Journal and issue number
4.) DOI reference with URL link to the article
5.) Abstract in quotes
6.) Your hopefully minimum one paragraph review commenting on your reading of the full-text article and anything exciting or fascinating you found within it.
7.) Optional: Attached pictures of some of the figures from the article

If you are having trouble accessing full-texts of papers, I would recommend you head to the local university with a flash drive and pick up whatever you want.

I would like to keep all articles within the range of the past 24 months, to keep everything recent.
Rules for sharing journal articles by Epsilon Alpha:

Several mods and users have brought up the idea of having a procedure of sharing of journal articles, and me and two of the other ADD mods have discussed this topic. As such, this is an experimental procedure to see how full text requests work out. Please leave comments/suggestions in this thread, we will do our best to make this as effective as we can; this is an experiment after all ;)

1) Do not post direct links to the paper, you can post that you are willing to send PM's of a specific paper(s) though.
2) Do not discuss the paper in the thread, make a separate thread or a relevant existing one to do so. This is to maintain an easily navigable request forum.
3) If you also would like the full text to a previously requested paper please PM the user who claims to have the fulltext or the user who requested it rather than post in the thread, however if you do not receive an answer within a reasonable time frame (~1 week) you can post a reply.

Request Format
Please link the pubmed or respective hosting service as well as post the abstact in a quote.
Chronic treatment with curcumin enhances methamphetamine locomotor sensitization and cue-induced reinstatement of methamphetamine self-administration.

Zhao C, Lou Z, Zimmer B, Yu Z, Li P, Ma B, Sun Y, Huang K, Zhou W, Liu Y.
Ningbo University School of Medicine, 818 Fenghua Road, Ningbo, Zhejiang 315211, PR China.
Curcumin, a major active component of Curcuma longa, possesses antidepressant effects that are mediated by the 5-HT system. However, little is known about the effect of curcumin on the behavioral consequences of methamphetamine (METH).
The subjects were male, adult Sprague-Dawley rats. In Experiment 1, the effects of 20 and 40 mg/kg curcumin (i.p.) on response rates and breakpoints of 0.06 mg/kg/infusion METH were evaluated. In Experiment 2, rats were self-administering METH for 10 days followed by a 14-day abstinence period. During the abstinence period, the animals were treated with DMSO, 20 or 40 mg/kg curcumin. All rats were then tested for extinction responding and cue-induced reinstatement. In Experiment 3, rats were treated with DMSO, 20, or 40 mg/kg curcumin 15 min before a METH-induced locomotor activity test for 14 consecutive days. In Experiment 4, rats were pretreated with DMSO or curcumin (20 mg/kg or 40 mg/kg) for 13 days and were subsequently tested for METH-induced locomotor activity on the 14th day. In Experiment 5, three groups were tested for locomotor activity after an injection of DMSO, 20, or 40 mg/kg curcumin. The test was repeated for 14 days.
Curcumin produced little effect on response rates and breakpoints maintained by METH. Chronic treatment of only 40 mg/kg curcumin during the abstinence phase enhanced cue-induced reinstatement of METH self-administration. Chronic administration of curcumin increased METH-induced sensitization of locomotor activity at the lower (20 mg/kg) but not higher (40 mg/kg) dose. However pretreatment of curcumin alone showed no significant effect on acute locomotor responses to METH and locomotor responses per se.
Curcumin enhanced, rather than inhibited the behavioral effects of METH.
Copyright © 2012 Elsevier Inc. All rights reserved.
PMID: 22750063 [PubMed - indexed for MEDLINE]
Last edited by a moderator:
this sounds great.
I lack expertise in the field, but i have uni journal access and would happily provide anyone with full texts.
Got the first and third article.
My uni lacks a subscription to Clinical Chemistry (It had a subscription, but it expired in 2005, apparently. the fuck).

How can I most easily distribute these? Clearly, they're too large for attachments on here.

I read it last year when it came out, it was a very good review.
@Smyth: Impossible to access the linked thread at ScienceMadness. Care to post a copy of the essential parts here?
Illicit gamma-hydroxybutyrate (GHB) and pharmaceutical sodium oxybate (Xyrem®): Differences in characteristics and misuse
Lawrence P. Cartera, Daniel Pardib, Jane Gorslinec and Roland R. Griffithsd
Drug and Alcohol Dependence 2009.04.012
There are distinct differences in the accessibility, purity, dosing, and misuse associated with illicit gamma-hydroxybutyrate (GHB) compared to pharmaceutical sodium oxybate. Gamma-hydroxybutyrate sodium and sodium oxybate are the chemical and drug names, respectively, for the pharmaceutical product Xyrem® (sodium oxybate) oral solution. However, the acronym GHB is also used to refer to illicit formulations that are used for non-medical purposes. This review highlights important differences between illicit GHB and sodium oxybate with regard to their relative abuse liability, which includes the likelihood and consequences of abuse. Data are summarized from the scientific literature; from national surveillance systems in the U.S., Europe, and Australia (for illicit GHB); and from clinical trials and post-marketing surveillance with sodium oxybate (Xyrem). In the U.S., the prevalence of illicit GHB use, abuse, intoxication, and overdose has declined from 2000, the year that GHB was scheduled, to the present and is lower than that of most other licit and illicit drugs. Abuse and misuse of the pharmaceutical product, sodium oxybate, has been rare over the 5 years since its introduction to the market, which is likely due in part to the risk management program associated with this product. Differences in the accessibility, purity, dosing, and misuse of illicit GHB and sodium oxybate suggest that risks associated with illicit GHB are greater than those associated with the pharmaceutical product sodium oxybate.

nice review paper.
6.) Your hopefully minimum one paragraph review commenting on your reading of the full-text article and anything exciting or fascinating you found within it.

everyone seems to be skipping this step
Well, my article of interest has almost hit the 24 month mark, but I still find it fascinating.

Preclinical and clinical findings indicate that a GABA(B) receptor agonist baclofen decreases cocaine use. The present study investigated the effects of the GABA(B) receptor antagonist (2S)-(+)-5,5-dimethyl-2-morpholineacetic acid (SCH 50911), the agonists baclofen and 3-aminopropyl(methyl)phoshinic acid (SKF 97541) and the allosteric positive modulator 3,5-bis(1,1-dimethylethyl-4-hydroxy-beta,beta-dimethylbenzenepropanol (CGP 7930) in cocaine-and food-maintained responding under a fixed ratio 5 schedule of reinforcement in male Wistar rats. The effects of the GABA(B) receptor ligands on cocaine (10 mg/kg)-induced discriminative stimulus in a two-lever, water-reinforced fixed ratio 20 task and on basal locomotor activity were also assessed. Baclofen (2.5-5 mg/kg), SKF 97541 (0.1-0.3 mg/kg) and CGP 7930 (30-100 mg/kg) decreased the cocaine (0.5 mg/kg/injection)-maintained responding; SCH 50911 (3-10 mg/kg) was inactive in this respect. Baclofen (5 mg/kg) and SKF 97541 (0.3 mg/kg), but not CGP 7930 or SCH 50911 attenuated the food-maintained responding. The inhibitory effects of the GABA(B) receptor agonists and the modulator were blocked by SCH 50911. SKF 97541 (0.1 mg/kg) or CGP 9730 (30-100 mg/kg) did not produce a significant shift in the cocaine (1.25-10 mg/kg) dose-response curve in a drug discrimination procedure, while baclofen (1.5 mg/kg) or SCH 50911 (10 mg/kg) attenuated the effects of separate doses of cocaine. Baclofen (5 mg/kg) and CGP 7930 (100 mg/kg) significantly reduced basal horizontal activity. We found that pharmacological stimulation of GABA(B) receptors by direct agonists or allosteric positive modulation reduces cocaine reinforcement while this property of cocaine is not related to tonic activation of GABA(B) receptors. The GABA(B) receptor stimulation-induced reduction of cocaine reinforcement was separated from its discriminative stimulus effects. Moreover, a dissociation between effects of direct GABA(B) receptor agonists and a GABA(B) allosteric positive modulator on cocaine vs. food-maintained responding was demonstrated.

Filip, et. al. "Effects of GABA(B) receptor antagonist, agonists and allosteric positive modulator on the cocaine-induced self-administration and drug discrimination."
European Journal of Pharmacology, 2007 Nov 28;574(2-3):148-57.
PMID: 1769806

I'm particularly interested by Baclofen and related GABA-B agonist or positive allosteric modulators because they seem to be the first anti-craving medications, as they don't seem to affect subjective effects on cocaine. The authors explain at the end of the article that this is due to the inhibition of dopamine neurons in the VTA. I also found another reference of GABA-B localization (PMID: 14961561) that said GABA-B receptors are heavily expressed in the striatum and globus pallidus, which IIRC, are also involved with addiction. I'm excited that this could be a new area of research and focus for helping addicts, either alone or in combination with low-harm replacement therapies (methadone, bupe, etc.). I know there have been some conflicting human trials recently though, with one multi-center review saying that there was no benefit for using baclofen for cocaine addicts. I haven't looked into that review yet, but the authors suggest that the dose wasn't high enough. I'm just waiting for larger studies to come out, since most of the trials seem to enroll 40 or less people.

At the end of the article, the author mentions something about the GABA-B antagonist, SCH 50911 also reducing cocaine self-administration, which was confusing to me. Everywhere else in the article it seems as if SCH 50911 had no effect on cocaine SA, or it blocked the effects of baclofen on cocaine SA. Can anyone help explain this?

Also, I need a little help decrypting what they're talking about with the reduced food administration with the agonists. So baclofen and the positive allosteric modulators reduce food intake, but in the discussion it says that:

In contrast to the above findings, baclofen or CGP 44532 at
doses that reduced cocaine self-administration were without
significant effects on food-maintained responding on a discrete
trial procedure (Brebner et al., 1999; Roberts and Andrews, 1997)
or a multiple schedule of drug and food (Shoaib et al., 1998)in

Can anyone explain how these produces are different from the fixed ratio schedules that did show a reduction in food SA?
Last edited:
Also, I need a little help decrypting what they're talking about with the reduced food administration with the agonists. So baclofen and the positive allosteric modulators reduce food intake, but in the discussion it says that:

Can anyone explain how these produces are different from the fixed ratio schedules that did show a reduction in food SA?

I assume that the animals responded to a challenge offering them some kind of food reward, e.g. when a lever is pressed a snack is released that they really enjoy. While they may respond the same in terms of reward, their overall food intake of general meal may still be decreased.
Structure elucidation of a new designer benzylpiperazine: 4-bromo-2,5-dimethoxybenzylpiperazine.
Westphal F, Junge T, Girreser U, Stobbe S, Pérez SB.
Forensic Sci Int. 2009 May 30;187(1-3):87-96. Epub 2009 Apr 3.

Landeskriminalamt Schleswig-Holstein, Mühlenweg 166, 24116 Kiel, Germany. [email protected]

A new designer benzylpiperazine was seized in Germany for the first time. Interpreting the results of gas chromatography-mass spectroscopy (GC-MS), product ion spectroscopy (GC-MS/MS), and nuclear magnetic resonance (NMR) spectroscopy the compound was 4-bromo-2,5-dimethoxybenzylpiperazine. The structure of the new benzylpiperazine was finally proved by two-dimensional NMR correlations and by GC-MS after synthesis of two of the possible isomers from commercially available starting materials. Additionally mass spectroscopic data after liquid chromatography-mass spectroscopy (LC-MS/MS) using electrospray ionization (ESI) as well as ultraviolet (UV) spectral data of the new compound are presented. A small quantity of the new benzylpiperazine was seized in very high purity along with other also very pure designer drugs in Hamburg, Germany.

Last edited by a moderator:
Klein MT, Dukat M, Glennon RA, Teitler M. "Towards selective drug development for the human 5-HT1E receptor: a comparison of 5-HT1E and 5-HT1F receptor structure-affinity relationships." J Pharmacol Exp Ther. 2011 Mar 21.

The 5-HT1E receptor is highly expressed in the human frontal cortex and hippocampus, and this distribution suggests the function of 5-HT1E receptors might be linked to memory. To test this hypothesis, behavioral experiments are needed. Because rats and mice lack a 5-HT1E receptor gene, knockout strategies cannot be utilized to elucidate this receptor's function(s). Thus, selective pharmacological tools must be developed. The tryptamine-related agonist BRL54443 (5-hydroxy-3-(1-methylpiperidin-4-yl)-1H-indole) is one of few agents that binds 5-HT1E receptors with high affinity and some selectively; unfortunately, it binds equally well to 5-HT1F receptors (Ki≈1 nM). The differences between tryptamine binding requirements of these two receptor populations have never been extensively explored; this must be done in order to guide the design of analogs with greater selectivity for 5-HT1E receptors versus 5-HT1F receptors. Previously, we determined the receptor binding affinities of a large series of tryptamine analogs at the 5-HT1E receptor; we now examine the affinities of this same series of compounds at 5-HT1F receptors. The affinities of these compounds at 5-HT1E and 5-HT1F receptors were found to be highly correlated (r=0.81). All high-affinity compounds were full agonists at both receptor populations. We identified BODMT (5-n-butyryloxy-DMT) as a novel 5-HT1F receptor agonist with >60-fold selectivity versus 5-HT1E receptors. There is significant overlap between 5-HT1E and 5-HT1F receptor orthosteric binding properties; thus, identification of 5-HT1E-selective orthosteric ligands will be difficult. The insights generated from this study will inform future drug development and molecular modeling studies both for 5-HT1E and 5-HT1F receptors.

This is an interesting study because it contains some biochemical data about novel tryptamine derivatives and it also gives high affinity ligands for the the 5HT1E receptor, which is highly expressed and which also, up to now, selective ligands were not available for.

Free full text here: http://jpet.aspetjournals.org/content/early/2011/03/21/jpet.111.179606.long
There's a bunch of papers/journal articles (50 or so I'd say) mostly related to NMDAr/sigma/CB1/5ht2a/5ht1a and QSAR thereof on my server, I'd post a link if people wanted. Dunno about reviewing each and every one though.
Cool, I'll see about putting together a little index with abstracts or something today. I'm a little iffy about just posting links to a directory full of synthesis PDF's.

[edit]: Nope, upon further consideration, information wants to be free etc.
Here's some light bedtime reading, there's a few papers that really stick out.

Among others is a paper stating "A3A Methano" - remember that? - was nothing but toxic. Fucking RC vendors.

There's notable ones regarding hypericin and its sigma affinity and the antidepressant role they play.
Last edited:
An animal model of schizophrenia based on chronic LSD administration: old idea, new results.
Marona-Lewicka D, Nichols CD, Nichols DE.
Neuropharmacology. 2011 Sep;61(3):503-12. Epub 2011 Feb 23.
Many people who take LSD experience a second temporal phase of LSD intoxication that is qualitatively different, and was described by Daniel Freedman as "clearly a paranoid state." We have previously shown that the discriminative stimulus effects of LSD in rats also occur in two temporal phases, with initial effects mediated by activation of 5-HT(2A) receptors (LSD30), and the later temporal phase mediated by dopamine D2-like receptors (LSD90). Surprisingly, we have now found that non-competitive NMDA antagonists produced full substitution in LSD90 rats, but only in older animals, whereas in LSD30, or in younger animals, these drugs did not mimic LSD. Chronic administration of low doses of LSD (>3 months, 0.16 mg/kg every other day) induces a behavioral state characterized by hyperactivity and hyperirritability, increased locomotor activity, anhedonia, and impairment in social interaction that persists at the same magnitude for at least three months after cessation of LSD treatment. These behaviors, which closely resemble those associated with psychosis in humans, are not induced by withdrawal from LSD; rather, they are the result of neuroadaptive changes occurring in the brain during the chronic administration of LSD. These persistent behaviors are transiently reversed by haloperidol and olanzapine, but are insensitive to MDL-100907. Gene expression analysis data show that chronic LSD treatment produced significant changes in multiple neurotransmitter system-related genes, including those for serotonin and dopamine. Thus, we propose that chronic treatment of rats with low doses of LSD can serve as a new animal model of psychosis that may mimic the development and progression of schizophrenia, as well as model the established disease better than current acute drug administration models utilizing amphetamine or NMDA antagonists such as PCP.

This is not really earthshattering research or anything, but it is interesting to see that administration of LSD to young rats over extended periods of time induces prolonged psychosis. This provides some support of the permanent effect of psychedelic drugs as HPPD.