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Ketamine salts solubility

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Functional assays revealed that 5-APB and 6-APB were potent full agonists at 5HT2B receptors.
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Not good for the ol' heart valves then?
 
So here it's looking at the transporter affinity only but we know the primary action of MDMA, for example is as a releaser.

This means that the transporter affinities are a middle value where they can cause release without shutting down the transporter and preventing release into the synapse?
 
No, I think affinity for the transporter protiens is unrelated toi the ability of drugs to reverse transport. For instance drugs like citalopram have a humongous affinity for SERT but do not cause release, and drugs like MDMA have compartatively less affinity but elevate serotonin concentrations much more effectively.
 
Hi first time on site. if someone had som very clean wizz amphetamine. Is there a simple way to turn it in to ice
 
There is, but it's not simple, nor would the average lay-man be able to do it.
Also, we don't discuss synthesis on this board.
 
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"i am become death, destroyer of worlds" -- j robert oppenheimer

"When you see something that is technically sweet, you go ahead and do it and you argue about what to do about it only after you have had your technical success. That is the way it was with the atomic bomb."
 
Preclinical Safety Assessment of the 5-HT2A Receptor Agonist PET Radioligand [11C]Cimbi-36

Progress on use of 25B-NBOMe as a radioligand for PET scanning

[11C]Cimbi-36 was recently developed as an agonist radioligand for brain imaging of serotonin 2A receptors (5-HT2A) with positron emission tomography (PET). This may be used to quantify the high-affinity state of 5-HT2A receptors and may have the potential to quantify changes in cerebral 5-HT levels in vivo. We here investigated safety aspects related to clinical use of [11C]Cimbi-36, including radiation dosimetry and in vivo pharmacology.
 
Not that recent, but reading the story in pd of some guy going blind after tripping had me remembering it.
http://www.ncbi.nlm.nih.gov/pubmed/19221973
[Recurrent cortical blindness after LSD-intake].

Recurrent disturbances of vision associated with headaches are typical signs of a migraine. A 15-year-old girl suffered from common migraine. The patient had a headache and nausea five days after a first and proved intake of LSD. Shortly later, a complete blindness of both eyes developed within seconds. These symptoms continued for 48 hours. As the pupillar reactions were intact the findings were consistent with cortical blindness. MRI and MR-angiography of the brain, analysis of the cerebrospinal fluid and blood investigations for thrombophilia were normal. The EEG showed a bilateral symmetrical delta wave slowing over the occipital areas. Within the following three months the girl had three more episodes with complete blindness over a period of 12-36 hours. There have never been any visual disturbances in between the episodes and afterwards. Extended diagnosis with long term blood pressure measurement, Doppler sonography and visual evoked potentials were normal. The occipital slowing in the EEG persisted for 18 months. As the symptoms were unusually long and severe for a complicated migraine it is possible that the temporary blindness was the correlate of flash backs caused by the LSD. LSD intake could trigger additional, local cortical dysfunction (e. g. in the occipital areas) in preexisting migraine.
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This review is almost a year old now, but I saw there was some interest in depressogenic substances so I'll just leave this here.

CB1 receptor antagonists: new discoveries leading to new perspectives.
http://www.ncbi.nlm.nih.gov/pubmed/22463610

Abstract
CB(1) receptor antagonists were among the most promising drug targets in the last decade. They have been explored and found to be effective as therapeutic agents for obesity and related cardiometabolic problems; however, use of rimonabant, the first marketed CB(1) receptor antagonist, has been suspended because of its anxiogenic and depressogenic side effects. Because some other antiobesity drugs, like dexfenfluramine or sibutramine, were also suspended, the unmet need for drugs that reduce body weight became enormous. One approach that emerged was the use of CB(1) receptor antagonists that poorly cross the blood brain barrier, the second, the development of neutral antagonists instead of inverse agonists, and the third, use of personalized medicine, namely the selection of the patient population without psychiatric side effects. In this review, we dissect the peripheral and central mechanisms involved in the effects of CB(1) receptor antagonists and argue that central mechanisms are more or less involved in most cardiometabolic therapeutic effects and thus, among patients with unsatisfactory therapeutic response to compounds with peripheral action, centrally acting antagonists may be needed. An analysis of pharmacogenetic factors may help to identify persons who are at no or low risk for psychiatric adverse effects. Here, we present the models and identify molecular mechanisms and receptors involved in the effects of stress-, anxiety- and depression-related neurocircuitries sensitive to CB(1) receptor antagonists, like the serotonergic, noradrenergic and dopaminergic systems, which are not only regulated by CB(1) receptors, but also regulate the synthesis of the endocannabinoid 2-arachidonoyl-glycerol.
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Design, Synthesis, and Pharmacological Characterization of N- and O-Substituted 5,6,7,8-Tetrahydro-4H-isoxazolo[4,5-d]azepin-3-ol Analogues: Novel 5-HT2A/5-HT2C Receptor Agonists with Pro-Cognitive Properties
http://dx.doi.org/10.1021/jm301656h

Interesting new scaffold for 5-HT2A/2C agonists.

The isoxazol-3-one tautomer of the bicyclic isoxazole, 5,6,7,8-tetrahydro-4H-isoxazolo[4,5-d]azepin-3-ol (THAZ), has previously been shown to be a weak GABAA and glycine receptor antagonist. In the present study, the potential in this scaffold has been explored through the synthesis and pharmacological characterization of a series of N- and O-substituted THAZ analogues. The analogues N-Bn-THAZ (3d) and O-Bn-THAZ (4d) were found to be potent agonists of the human 5-HT2A and 5-HT2C receptors. Judging from an elaborate pharmacological profiling at numerous other CNS targets, the 3d analogue appears to be selective for the two receptors. Administration of 3d substantially improved the cognitive performance of mice in a place recognition Y-maze model, an effect fully reversible by coadministration of the selective 5-HT2C antagonist SB242084. In conclusion, as novel bioavailable cognitive enhancers that most likely mediate their effects through 5-HT2A and/or 5-HT2C receptors, the isoxazoles 3d and 4d constitute interesting leads for further medicinal chemistry development.
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jm-2012-01656h_0010.gif
 
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Shambles said:
Two atoms are walking down the street together. The first atom turns and says, "Hey, you just stole an electron from me!"

"Are you sure?" asks the second atom.

To which the first atom replies, "Yeah, I'm positive!"

<3
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heh
 
Hey everybody. I usually just lurk around BL, every now and then post a question in OD, but im not too actively involved, but i want to be! I am a chem/pre-pharm major but at the moment my chemistry and pharmacology knowledge is pretty limited. So i was wondering if anybody here could help me learn the basics on these topics. I know how to draw out some simple compounds and stuff using their IUPAC names and stuff like that, but what really confuses me is how their structures determine a drugs effects? how does that work?!
 
I think you'll probably have a lecture course on that, and even then you could take another and still only have scraped the surface!

I recommend khan acadamey for the basic stuff, and occasional courses on coursera for the more specialised stuff.
 
i found some neat papers on Tocris' website.

http://www.tocris.com/pdfs/pdf_downloads/receptor_binding_review.pdf - Review on Ki and how it is measured, receptor binding, etc

http://www.tocris.com/pdfs/pdf_downloads/5-HT_Receptors_Review.pdf - Tocris Bioscience review on the serotonin receptors (5ht 1 family, 5ht2family, & 5ht3)
http://www.tocris.com/pdfs/pdf_downloads/dopamine_receptors_review.pdf - Dopamine receptors
http://www.tocris.com/pdfs/pdf_downloads/gaba_receptors_review.pdf - GABA, benzos, neuroactive steroids.
http://www.tocris.com/pdfs/pdf_downloads/opioid_receptors_review.pdf - Opioids
http://www.tocris.com/pdfs/pdf_downloads/melatonin_receptors_review.pdf - Melatonin MTx receptors
 
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