• N&PD Moderators: Skorpio | thegreenhand

Erowid/BlueLight Neuropharmacology Text

What is a neuron?

What is a neuron?

The most important properties of a neuron is its ability to fire an action potential and to release neurotransmitters. Anatomically, a neuron is analogous to a tree: it has roots in the form of a huge number of of branching dendrites (the receiving end of a neuron), it has a trunk, in the form of an axon (the transmitting section of a neuron) and a branches, in the form of axonal arborizations or terminals (Fig 1 and 2). Generally, a neuron can be seen as an integrator and disseminator of information. Figure 2 shows a real image of a single neuron filled so it can be visualize independently of the hundreds of neurons surrounding it. This image shows the dendritic spines of a dendrite (the small dots along the length of many of the dendrites). Each of those these spines will make at least one connection (or synapses) with a neighboring neuron, there will also be many synapses which we can not see, this means that this neuron makes thousands of connections with other neurons. Although we can not see it’s axonal terminals, it is safe to assume that this cell then makes thousands of connections with other neurons. Hence a neuron both receives inputs from a huge number of neurons, as well as giving inputs to a large number of neurons.

neurondiagram.gif

Figure 1. Schematic of a neuron

luciferase-neuron.jpg

Figure 2. Micrograph of a filled neuron, probably a hipocampal pyramidal cell. Neuron image thanks to www.lebenswissen.de/pix/ Dendritic spine image thanks to tonto.stanford.edu/~viktor/

Functionally, a neuron is similar to a piece of wire, with a few changes. For one, information is generally only sent in one direction. Neurotransmitters are chemicals that are released by neurons in order to send signals to other neurons. Neurotransmitters are released by the axonal terminals of one cell, and diffuse across the synapse to the dendrites of another cell. Here neurotransmitters can bind to “receptors” and effect the neuron in many ways, but importantly they can alter the probability of it firing an “action potential”, the electrical signal which neurons send over long distances. These principles are discussed further in the “electrical properties of the neuron” and the “chemical properties of the neuron” chapters.

Another difference between a neuron and a piece of wire, is that a neuron can alter the nature of the information it is going to transmit depending on previous signals it has received, that is to say, it is not a passive conductor but a small processor, capable of making decisions. There are some 100 billion neurons in the brains of humans. Each one making and receiving thousands of connections. This results in an unfathomable number of connections and pathways, signals can move through the brain in. Integrative processing allows the overwhelming depth of information received by the sensory organs to be processed into discrete, meaningful perceptions. Conversely, the dissemination of information allows for associative processes to occur. These principles are discussed further in the “signaling properties of neurons”
 
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I'll do both proposed sections on signaling properties of neurons.

Also, I will write brief sections on the functions of the major neurotransmitters in brain. I think the learning and memory portion can perhaps be put in the section for glutamate, because anything but the simplest mechanistic discussion of synaptic plasticity is too technical for the layman.
 
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I don't think functional discussion of neurotransmitters is really that constructive... functionallity is a function of release style, location of release, and receptor function... as well as g-protein trafficing... still, if you've got time to get into learning and memory (which hopefully should entail how addiction is just an abarant learning process) and how neurons alter each others signalling mechanism, potentially getting into burting, versus tonic, versus exclusively evoked neuronal firing patterns... Sure man... write something... anyone, write something...
 
G-protein coupled receptors and signalling pathways

G-protein coupled receptors (GPCRs) are found in all animals so far investigated and even many plants and make up the single largest gene family in the human genome, indicating their importance as mediators of cell signaling. GPCRs should be of great interest to anyone investigating recreational drugs, as, for instance all of the opioid receptors, all of the 5 dopamine receptors, all of the 9 adrenoreceptors and all but 1 of the 13 or more serotonin receptors are GPCRs. GPCRs are large proteins that exist in the outer membrane of cells, with part of their protein exposed to the extracellular side (so that ligands can bind) and part of the protein facing the intracellular side (so that the receptor can effect the cell). GPCRs gain their name from their ability to bind to and activate guanine nucleotide-binding protein (G-proteins). These G-proteins allow the receptor to amplify the initial signal and effect many intracellular systems.

G-proteins are a complex of three separate subunits, called alpha, beta and gamma. The alpha subunit of the G-protein binds a guanine nucleotide: guanosine triphosphate (GTP) when the subunit is active and guanosine diphosphate (GDP) when the subunit is inactive. When an GPCR is in it’s neutral, non-active, agonist free state, it is not associated with a G-protein, however, when the GPCR becomes active because of agonist binding, the conformation of the GPCR is such that a G-protein can bind to its intracellular side. Once a G-protein binds to a GPCR it enhances a conformational change in it alpha-subunit, which causes the G-protein to release its molecule of GDP and bind a molecule of GTP. Now the G-protein dissociates from the GPCR and splits in two: into the alpha subunit and a beta-gamma subunit complex. These activated subunits can now alter the activity of many “effector systems”, for instance the GTP containing alpha subunit can effect many enzymes and proteins, while the beta-gamma complex often directly effects the activity of many ion channels and enzymes (fig. 1). If a G-protein activated effector system produces a molecule which continues the signaling cascade, then the molecule is called a 2nd messanger. The alpha subunit catalyses the breakdown of GTP of GDP, when this occurs the alpha subunit rebinds to the beta-gamma complex, ceasing both of their abilities to activate effector systems.

GPCRcylce.gif

Figure 1. The cycle of G-protein coupled receptors and their assocaited G-proteins

When a GPCR is activated by an agonist, as mentioned, G-proteins can bind, but this process is not limited to a single G-protein, indeed, as long as an agonist remains bound to GPCR it can activate many G-proteins. Likewise, the active forms of the alpha and beta-gamma subunits of the G-protein can activate many effector proteins. Furthermore, if the effector protein is an enzyme, each enzyme can produce a huge number of products while it is being activated by the G-protein subunits. This means that for a single agonist binding, a huge amplification of the signal can be transduced into the intracellular environment.

G-proteins and hence GPCRs can effect a huge variety of proteins, but there is specificity in their actions. The alpha subunits of G-proteins are not always the exact same kind of protein, indeed, there are over 20 varieties of alpha subunit (and there is a growing body of literature about multiple subtypes of beta and gamma subunits). The alpha subunits are usually sorted into 4, functionally different families, with each family containing anywhere from 2 to 9 different alpha subtypes. The families are alpha-s, alpha-i, alpha-q and alpha-12. G-proteins are generally named after the alpha subunit they contain, so that a G protein containing alpha-s is called G-alpha-s, or just G-s. These alpha families generally effect the same effector systems, alpha-s subtypes generally stimulate the enzyme “adenylyl cyclase”, alpha-i subtypes inhibit adenylyl cyclase and inhibit presynaptic Ca2+ channels, alpha-q subtypes stimulate the enzyme phospholipase C and alpha-12 effects various novel intracellular targets.

Different GPCRs have different affinities for G-proteins made up of different alpha subunits, so that some GPCRs will only couple to a particular G-protein. On the other hand many GPCRs couple to several kinds of G-proteins. Furthermore, in receptors that couple to two or more kinds of G-proteins, different agonists can cause the GPCR to activate a particular G-protein over other kinds, a processes called “agonist-directed trafficking”. For instance the serotonin 5-HT2A receptor has been shown to couple to G-alpha-q, G-alpha-12 and possibly the novel G-alpha-13. When serotonin binds to the 5-HT2A receptor it causes a roughly even activation of G-alpha-q and G-alpha-12, but psilocin activates G-alpha-12 roughly 25 times more readily.

Adenylyl cyclase (AC) is a very common enzyme, which converts the ubiquitous energy currency of the cell “ATP” into the 2nd messanger cyclic adenosine monophosphate (cAMP). cAMP activates kinases (enzymes which phosphorylate proteins); kinases which are activated by cAMP are fall into the protein kinase A (PKA) family, and regulate the activity of a huge number of receptors and ion channels especially (fig. 2). The effect of PKA on ion-channels can have profound effects on neuronal activity, for instance when a neuron is strongly excited (depolarized) it will generally fire action potentials in rapid succession, but the rate of firing will slow and after about 2 seconds firing will stop completely. This “accommodation” is due to the Ca2+ which enters the cell due to depolarization, activating calcium-activated potassium channels and hence positively charged potassium will leave the cell and attempt to repolarize the cell, preventing action potential formation. In certain cells, noradrenaline binding to beta-adrenoreceptors actives G-alpha-s G-proteins, which activates AC, which causes cAMP build up and activates PKA. PKA phosphorylates calcium-activated potassium channels, preventing accommodation. This means that cells which are strongly depolarized and exposed to noradrenaline (for instance, released by arousal or amphetamines) will continue to fire at a high frequency for a long time, where normally, they would fall silent.

Phospholipase C (PLC) is activated by G-alpha-q and it breaks down particular fats in the membranes of neurons into two 2nd messenger products: inositol triphosphate (IP3) and diacylglycerol (DAG). These two molecules effect two different, but often-complimentary systems, IP3 binds to intracellular IP3 receptors on compartments within the cell (i.e. endoplasmic reticulum) and cause them to release Ca2+. DAG on the other hand activates protein kinase C (PKC) a kind of Ca2+ dependent protein kinase. You can see then that the two signaling molecules produced by the action of G-alpha-q on PLC work synergistically to increase the activity of PKC, although the Ca2+ released by IP3 can have many other effects. PKC (and other Ca2+-dependent protein kinases) effect a huge number of protein targets, but of special interest to neuropharmacologists is their effects on ligand gated ion channels (fig. 2). One of the classical effects of PKC is to phosphorylate the NMDA glutamate receptor (See ligand gated ion channels), and this phosphorylation can enhance the effect of the NMDA receptor or paradoxically increase its rate of inactivation depending on the particular nature of the PKC cascade. PKC can also enhance or depress AMPA glutamate receptors and GABA-A receptors.

GPCRcascade2.gif

Figure 2. The signaling casaced of the three classical G-alpha subunits

As mentioned, the beta-gamma subunit complex can directly effect ion channels, the classic target being the so-called G-protein-coupled inwardly rectifying potassium (GIRK) channel. This class of potassium channel only opens when the cell is held at below –70mV, which stabilize the membrane potential by canceling any depolarizing (excitatory) currents by the opposing flow of K+ ions. This means that small excitatory inputs have no effect, and that larger currents are needed to raise the cell above –70mV, at which point excitatory inputs are much more efficient at exciting the cell. When the beta-gamma subunit complex binds to the GIRK channel it massive increase the current which can flow through them, meaning that an even larger excitatory current is needed to get the cell above the –70mV threshold needed to close the GIRK. Both the cannabinoid CB1 and Mu opioid receptor activate GIRK, though as both receptors act presynaptically, their effect is to reduce the Ca2+ influx at presynaptic terminals which induce transmitter release. In combination with the fact that both of these receptors couple to G-alpha-i containing G-proteins that directly inhibit Ca2+ channels, the end result of activation of these receptors is to reduce the amount of neurotransmitter released.

GPCRs also have many mechanisms for signaling to the nucleus of a cell, and hence to control gene expression, this area is still poorly understood, but probably effects many properties of the brain, such as receptor expression, propensity for learning and memory and cell division.
 
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how about 'what is the function significance of a.) diffuse modulatory neurotransmitter systems, and b.) what is all this talk about dopamine? (with regard to addiction and pleasurable sensations?)

sorry long time no see bilz0r, i've been working my ass off. i'm doing a paper this semester entitled 'the neurobiology of addiction' (set up as a conjunct between Michelle Glass and some people from the behavioural science department) its gonna be tight. ill start writing a bit for the book when i get some decent references and material from that.

(OT: i'm reading Céline's journey to the end of the night. its very much my style - i wish i could write like that)
 
Yeah, it's a good book that one.... Though the first half is much better than the second half.

yeah, the dopamine thing I'd like to get covered in the Learning and Memory section.. the diffuse/volume transmission section is something I'd like to cover in a special topic I want to write on amphetamines....

So are you ever gonna get around to written the section of Down regulation? It's something I don't know a whole heap about.... but I suppose the actual mechanism of down-regulation aren't as important as the functional consequences, though something on mechanisms might be helpful to help people understand how NMDA antagonists and other drugs could possibley help reverse tolerance.
 
*spoiler* (i'm not up to the second half yet...)

mm kappa antagonists reducing opoid tolerance etc..

i am uber busy at the moment. hopefully that will change soon - i only have classes 3 days a week this semester, but I will probably have quite a bit of ongoing work, so yeh hopefully i will get around to starting it within 3-4 weeks or so.
 
I would be happy to write the chapter on pharmacokinetics, including discussion and graphs of half-lives, steady-state metabolism, induction, inducers, plasma concentrations, oil/water partition coefficients, and drug-distribution.

Does anybody have any other topics within this subject they suggest I write about?

There should also be a section on the basic enzymes which are responsible for many of the metabolic breakdown pathways... Like glucuronization, oxidation, hydroxylation, etc... somebody else should do this part, because while I could look up all the enzyme names, I really don't have time for that.

I also would be happy to volunteer Wiki-space and webhosting, I'm involved in the Wiki developer community and could help you find the Wiki software which would be easiest to write a Neuropharmacology text with. Feel free to IM/email me about this.
 
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^ Yeah, that sounds great. If you covered the basics of pharmacokinetics, absorption (passive (oil/water, stomach contents) active (rare)), distribution(BBB permiability, plasma proteins), metabolism (enzymes(induction/inhibition) and excretion I think that would just be the best shit out.

I was thinking of putting the final thing on wikipedia... but I don't really know anything about that, I don't really like the idea of some punter coming along and fucking with it...
 
14BD: A GHB pro-drug, largely devoid of intrinsic activity.

2C-X: Chemicals such as 2C-B, 2C-I, 2C-E and 2C-T-7. These substitued phenethylamine hallucinogens have had little research devoted to them and nothing is known about their binding properties, though it is almost certain that they will be potent 5-HT2A receptor agonists. There is one paper show that 2C-I/B/D/H are 5-HT2A receptor antagonists, but this was demonstrated in a system which has little relevance to the complex nature of 5-HT2A receptor activation in the brain.

5-MeO-DMT: A tryptamine hallucinogen. It's hallucinogenic properties are attributed to its 5-HT2A receptor agonist effects though it is also a potent 5-HT1A receptor agonist.

Alcohol: See ethanol

Amphetamine: Cause the noradrenaline, dopamine and serotonin reuptake transporters to work in reverse (in that order of potency). Theses transporters normally take their respective neurotransmitter out of the extracellular fluid surrounding neurons and prevent them from binding to receptors, amphetamines cause the transporters to work in reverse, and move their neurotransmitters out of the cell, into the extracellular fluid. The action of amphetamines is dependent on them amphetamine passing through the transporter, hence the action of amphetamine is blocked reuptake inhibitors (like some antidepressants)

Benzodiazepines: A collection of pharmacologically and chemically related compounds which bind to the GABA-A ion channel, but at a site seperate to the GABA binding site. Benzodiazepines increase the affinity of the GABA-A receptor for GABA, and hence potentiate GABAs action.

Cannabidiol: Although often refered to as "non-psychoactive", cannabindiol is definately active. It has been shown to inhibit the anxiety inducing effects of THC [1] and be neuroprotective in many models of neurodegeneration. It has been consistantly shown that cannabidiol does not act on the CB1 receptor. It has been shown that cannadidiol acts by inhibiting the uptake and breakdown of the endogenous cannabinoid anandamide, but even if this action is replicated in vitro, the excess anandamide can not be acting on CB1 receptors. It has been hypothesised that Cannabidiol acts on the as yet uncharacterised cannabinoid receptor(s) which are speculated to exsist.

Cannabinoids: Cannabinoids are any of the chemically unique components in cannabis, though generally refers to psychoactive components. The classical cannabinoids are Ä9-tetrahydrocannabinol (THC), cannabinol (CBN) and cannabadiol (CBD).

Cannabinol: Another so called "non-psychoactive" cannabinoid. Reports show that it has very little or no psychoactive effects, though it definately has some physiological effects through unknown, non-CB1 receptor mechanisms. One report indicates it potentiates some of the effects of THC in humans[2].

Cocaine: Inhibitor of Dopamine, Serotonin and noradrenaline reuptake transporters, probably in that order of potency, leading to a higher level of these neurotransmitters in the extracellular fluid. Also blocks voltage sensitive sodium channels at low potency, which causes its local anaethetic action.

Codiene: A metabolic precursor of morphine (see opioids), converted to morphine by the liver enzyme CYP2D6.

DMT: One of the simplest members of the hallucinogenic tryptamine family. It's hallucinogenic activity is due to its agonist activity at 5-HT2A receptors, though it also has high affinity actions at 5-HT1A/D and 5-HT6 receptors, though not 5-HT1B receptors. It may have actions at other receptors, but these have not been studied at this time.

Ethanol: Alters the function of several ligand gated and voltage gated ion channels, including potentiating certain GABA-A receptors, certain nicotinic receptors, 5-HT3 receptors and glycine receptors while inhibiting NMDA receptors, voltage gated Ca2+, Na+ and K+ channels and certain nicotinic receptors. The most potent (and hence probably most important) actions of ethanol are potentiation of GABA-A receptor actions, inhibition of NMDA receptors, inhibition of voltage gated calcium channels and possibley potentiation of Nicotinic receptors.

Dextromethorphan: Classically known for its NMDA-receptor antagonist effects, it is actually a more potent serotonin reuptake transporter inhibitor. It also has significant potency for the sigma receptor. It is converted in the body, into dextrophan, which has a significantly higher NMDA receptor affinity.

GHB: Both an endogenous neurotransmitter and a recreational drug. GHBs highest affinity action is as an agonist at the GHB receptor, while it has a lower affinity action as an agonist at the GABA-B receptor. A lot of experimental results have indicated that the GABA-B receptor is the pharmacologically important target of GHB, but this is generally because the experimenters have used high doses of GHB and have recorded GABA-B dependent measures. It is likely that low doses of GHB in humans act primarily via the GHB receptor while higher, hynotic doses act via GABA-B.

GBL: A GHB prodrug, but as well is a more potent GABA-B receptor agonist

Heroin: See opioids

LSD: A prototypic indole hallucinogen. It's recreational, hallucingenic effect is largley due to its 5-HT2A receptor (partial) agonist effect. It also has marked affinity for 5-HT1A/B/E/F, 5-HT2B/C, 5-HT5A/B, 5-HT6, 5-HT7, D1, D2, D3, D4, D5, and alpha1A/B receptors. These effects on other receptors may explain LSDs unique potency and nature.

Ketamine: A dissociative anaethetic best known for its potent non-competative NMDA receptor antagonist effects. It has also been shown to be a sigma, 5-HT2[3], D2[3,4] and a relatively very weak (~20µM) kappa opioid receptor agonist (PDSP data)

MDMA: An amphetamine which is about ten times more specific for releasing serotonin and noradrenaline than dopamine, though it probably still causes significant dopamine release through the serotonin it releases activating 5-HT2 receptors on dopaminergic cells or cells which control the firing of dopaminergic cells. MDMA itself is relatively weak at the 5-HT2A receptor (100x weaker than its actions at monoamine transporters)[5]

Methamphetamine: An amphetamine which causes the release of noradrenaline, dopamine and serotonin (in that order of potency). Methamphetamine is probably more potent that amphetamine because it is less suceptable to metabolism and more rapidly pentrates into the brain.

Morphine: See opioids

Nicotine: Active chemical in tobacco. Nicotinic binds to a wide variety of nicotinic acetylcholine receptors (ligand gated Na+ channels). Nicotine binds with high affinity to α4β2 nicotinic receptor although evidence indicates that it is the (α4)2α5(β2)2 and α4α6α5(β2)2 nicotinic on dopaminergic neurons that causes the addictive profile of nicotine [6].

Nitrous Oxide: Like most gaseous anaethetics, it's actions are somewhat of a mystery. It is likely that nitrous oxide's analgesic effects are somehow caused by the release of endogenous opioids, though its dissociative action are probably a mix of actions on ion channels (like those mentioned for ethanol).

Opioids: Any drug which shares a significant pharmacological similarity with morphine. Distinguished from "opiates" which are chemicals found in opium. Pharmacologically, opioids which are used recreationally have potent Mu-opioid receptor agonist effects, however most are non-specific agonists are all opioid receptor subtypes.

Oxymorphone/oxycodone: See opioids

Salvia/Salvinorin: Salvia is a plant containing a large number of alkaloids and non-alkaloids, the most famous of which is Salvinorin A, which is a selective Kappa opioid agonist. It is believed that this is the mechanism for salvias psychedelic action.

THC: The architypal cannabinoid. A potent agonist at CB1 and CB2 cannabinoid receptors as well as actions which can not be atributed to either of those receptors.

1. Zuardi AW, Cosme RA, Graeff FG, Guimaraes FS: Effects of
ipsapirone and cannabidiol on human experimental anxiety. J
Psychopharmacol 1993;7:82-88.

2. Karniol IG, Shirakawa I, Takahashi RN, Knobel E, Musty RE.
Effects of delta9-tetrahydrocannabinol and cannabinol in man.
Pharmacology. 1975;13(6):502-12.

3. Kapur S, Seeman P.
NMDA receptor antagonists ketamine and PCP have direct effects on the dopamine D(2) and serotonin 5-HT(2)receptors-implications for models of schizophrenia.
Mol Psychiatry. 2002;7(8):837-44

4.Seeman P, Ko F, Tallerico T.
Dopamine receptor contribution to the action of PCP, LSD and ketamine psychotomimetics.
Mol Psychiatry. 2005 (epub)

5. Nash JF, Roth BL, Brodkin JD, Nichols DE, Gudelsky GA.
Effect of the R(-) and S(+) isomers of MDA and MDMA on phosphatidyl inositol turnover in cultured cells expressing 5-HT2A or 5-HT2C receptors.
Neurosci Lett. 1994;177(1-2):111-5

6. Wonnacott S, Sidhpura N, Balfour DJ.
Nicotine: from molecular mechanisms to behaviour.
Curr Opin Pharmacol. 2005 Feb;5(1):53-9
 
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who mE, i am very excited about the chapter you are writing. I can't wait to read it. It would answer many of my questions. :)
 
Hmm... can't believe this hasn't been finished yet. There's so many knowledgable people on bluelight...

I'll try to write a short chapter about proteins:


-What is a Protein?
Proteins are a certain type of biopolymers/biomacromolecules (molecules that are made out of very many components and therefore have a large molecular weight). They consist of the following elements: Carbon, Hydrogen, Oxygen, Nitrogen and Sulfur.
Every cell is made out of proteins and proteins are made out of amino acids chains that are interconnected by so called peptid bonds (Carbon-Nitrogen bonds). Peptid bonds can be broken down by making the proteins react with water. Since this process is very slow it is usually accelerated by enzymes (which are in fact, also proteins).
There are 20 different amino acids that proteins can consist of. The length of those "polypeptid chains" can be as short as less than 20 amino acids or as long as several thousand amino acids. This enables the proteins to have a large variety of functions. To mention just a few of them, they can function as enzymes, enable the muscles to contract or control many body processes as hormones.

Feel free to add or modify any information that you feel is missing or incorrect.
 
^ Thanks for contributing crook, says pretty much everything... If any of you other lazy sods wants to edit it, or add something or whatever... go ahead.
 
Thx, I was afraid I forgot sth. So get off your lazy asses and write another chapter, all you chemist or whatever bluelighters.

crOOk
 
for everybody's info... I'm being lazy cause I've got lots of other crap to do like look for a job and an apartment and do homework and work on consulting gigs... but I'll do my pharmacokinetics chapter *eventually* (lets say... by sept 1!)

*edit* got even lazier
 
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I'm new here, but I think this is an excellent idea. I have a very limited background in cell bioliogy and very little knowledge of pharmokinetics and the like, but if needed, I might be able to help create a few diagrams here and there?

//Moracca
 
W00T! Great first post moracca!!!

@who mE?
He, we're all busy dude, working, school, house work etc. :p Can't wait for your chapter though. Btw are you coming to the voov or not?

crOOk
 
Thanks! I just came across the site today when it was referenced on another forum, and it seems like there are some very intelligent discussions that go a little deeper into how drugs work, which is a topic i'm very eager to learn more about. Anyhow, let me know if I can be of service in any way. I look foreward to expanding my mind on the bluelight forums.

//Moracca
 
W00T! Another member! Dude, check it out, bluelight is a whole community with journals, galleries and shit unlike other forums. It's the shit.

crOOk
 
Two things....

1) the likely audience for this writing is probably people who are semi-educated... in the sense that they probably know a few things about cells, chemistry etc., but have never heard of the likes of allosteric modulation or don't know that an agonist and antognist are not really 'true opposites' etc. In that vein, it might be a good idea to have some links and/or suggested reading that is not right out of discipline specific journals. Two books spring to mind; one pretty much 5HT specific, and the other very broad and in-depth, but still primarily aimed at a lay audience. "Trips: How Hallucinogens Work In Your Brain" by Cheryl Pellerin & "Essential Psychopharmacology: Neuroscientific Basis and Practical Applications" by Stephen M. Stahl, M.D., Ph.D. I am sure there are others as well, but the Stahl book is pretty comprehensive considering it's target audience.

2) regarding receptor profiles; I know that the NIMH-PDSP (National Institute of Mental Health Psychoactive Drug Screening Program) recently screened 19 psychedelic drugs against a large panel of receptors etc. Many of these were newer RCs. This list was something along the lines of 2C-B, 2C-B-fly, DOB, DOI, DOM, 2C-E, 2C-T-2, ALEPH-2, Mescaline, MEM, MDA, MDMA, DMT, 5-MeO-DMT, 5-MeO-MIPT, DIPT, 5-MeO-DIPT, DPT, & Psilocin if I recall. So there is actually quite comprehensive data out there on the likes of 2C-T-2 and even 2C-B-FLY regarding their receptor affinities and effects on transporters and ion-chanels. I am just not sure where the nitty-gritty data has been published, if indeed it has.

OK that's it. I hope this might be helpful in some way and I will get out of the way now. Please dont feel the need to de-rail the thread flaming me if I have proved a hinderence.
 
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