Talk:Reuptake inhibitor

This is the talk page for discussing improvements to the Reuptake inhibitor article.
This is not a forum for general discussion of the article's subject.

Put new text under old text. Click here to start a new topic.
New to Wikipedia? Welcome! Learn to edit; get help.

Article policies

Find medical sources: Source guidelines · PubMed · Cochrane · DOAJ · Gale · OpenMD · ScienceDirect · Springer · Trip · Wiley · TWL

Pharmacology Mid‑importance

	This article is within the scope of WikiProject Pharmacology, a collaborative effort to improve the coverage of Pharmacology on Wikipedia. If you would like to participate, please visit the project page, where you can join the discussion and see a list of open tasks.PharmacologyWikipedia:WikiProject PharmacologyTemplate:WikiProject Pharmacologypharmacology articles
Mid	This article has been rated as Mid-importance on the project's importance scale.

Neuroscience Low‑importance

	This article is within the scope of WikiProject Neuroscience, a collaborative effort to improve the coverage of Neuroscience on Wikipedia. If you would like to participate, please visit the project page, where you can join the discussion and see a list of open tasks.NeuroscienceWikipedia:WikiProject NeuroscienceTemplate:WikiProject Neuroscienceneuroscience articles
Low	This article has been rated as Low-importance on the project's importance scale.

Molecular Biology: MCB

	This article is within the scope of WikiProject Molecular Biology, a collaborative effort to improve the coverage of Molecular Biology on Wikipedia. If you would like to participate, please visit the project page, where you can join the discussion and see a list of open tasks.Molecular BiologyWikipedia:WikiProject Molecular BiologyTemplate:WikiProject Molecular BiologyMolecular Biology articles
???	This article has not yet received a rating on the importance scale.
	This article is supported by the Molecular and Cell Biology task force (assessed as Low-importance).

Medicine High‑importance

	Medicine portal This article is within the scope of WikiProject Medicine, which recommends that medicine-related articles follow the Manual of Style for medicine-related articles and that biomedical information in any article use high-quality medical sources. Please visit the project page for details or ask questions at Wikipedia talk:WikiProject Medicine.MedicineWikipedia:WikiProject MedicineTemplate:WikiProject Medicinemedicine articles
High	This article has been rated as High-importance on the project's importance scale.

Types category explanations?

I have never seen those agents being categorized like this, in most context NRI DRI SRI are all regarded none-selective.

And I can't understand why is agonist/antagonist subtypes of reuptake inhibitor. But this is not my profession so I am not sure, can anyone clarify? Thanks. ---Panintelize (talk) 08:15, 1 January 2016 (UTC)[reply]

DRI, NRI, and SRI were probably listed under selective in order to list and link to the hybrid reuptake inhibitor pages (SNRI, DNRI, SDNRI, etc). This categorization doesn't necessarily imply that all DRI, NRIs, and SRIs are selective inhibitors. Even so, I've removed the selective/nonselective grouping. The agonist/antagonist grouping was likely based upon the effect of associated reuptake inhibitors on neurotransmission (promoting/inhibiting, respectively). That classification isn't accurate for VMAT inhibitors that also promote neurotransmitter release at the plasma membrane (e.g., amphetamine, phenethylamine, methamphetamine, etc), so I removed that grouping as well. (Seppi333 (Insert 2¢) 19:58, 1 January 2016 (UTC)[reply]

Many errors in mechanism of action

for Allosteric site transporter substrates:

fluoxetine have no affinity to monoamine transporters(can't find such info in ref)

this is the only relevant info I can find about the allosteric site affinity of fluoxetine:

In addition, it acts as a positive allosteric modulator of the GABAA receptor at high concentrations, and norfluoxetine does the same but more potently, actions which may be clinically-relevant.[69] ----from fluoxetine with verifiable ref

and GABA's not monoamine.

from one of the ref:

the present study was directed at determining whether R-citalopram modifies the action of selective serotonin reuptake inhibitors (SSRIs) known to act on allosteric sites namely escitalopram, and to a lesser extent paroxetine, compared to fluoxetine, which has no affinity for these sites.

there seem to be problems with other agent listed in this section, too. But I have no time to check them thoroughly now.

Types:

mentioned in another topic. Panintelize (talk) 15:31, 1 January 2016 (UTC)[reply]

I removed fluoxetine from the section, per the ref you quoted. Seppi333 (Insert 2¢) 20:07, 1 January 2016 (UTC)[reply]

"leading to an increase in the extracellular concentrations of the neurotransmitter and therefore an increase in neurotransmission"

Inhibiting the reuptake process leads to decreased neurontransmission, because, Inhibiting the process of generating neurontransmitter transporters has no bearing on neurotransmissions, because, the process of generating neurontransmitter transporters only serves to generate neuron transmitter transports. not neuron transmitters.

This should read: Leading to a DECREASE in the extracellular {nothing}

An increase in extracellular concentrations of the neurotransmitter? We are talking about reuptake, which IS ABOUT NEURON.TRANSMITTER.TRANSPORTERS — Preceding unsigned comment added by Parkerrush92 (talk • contribs) 13:30, 15 June 2017 (UTC)[reply]

Inhibiting a process of recycling neurotransmitters. "is the reabsorption of a neurotransmitter by a neurotransmitter transporter of a pre-synaptic neuron after it has performed its function of transmitting a neural impulse."** reabsorption, does not specify replication, or any other process of generating more of anything. — Preceding unsigned comment added by Parkerrush92 (talk • contribs) 13:45, 15 June 2017 (UTC)[reply]

- - noted changes in lines and presentation during process. I do not care anymore. Goodbye. Wait, Yes I do. Get Pfizer? bye. Oh wait, I can't afford an attorney? Anybody there an attorney?

"controlled knowledge" Tapwater is a gay bomb.

Ok, sanity restored. I have since had a conversation. The increased prevelance in seratonin transmission is true, through the reuptake inhibition process is true. The probelem in efficacy occurs, because, seratonin is a transmittor, not itself a tranmission )context of synaptic expression. Reuptake inhibition leads to increased prevolance of seratonin, a transmittor. Increased transmittors in a transmission process is uselss, because transmittors transmit, and synaptic transmition transmits the chemical seratonin, an transmittor. — Preceding unsigned comment added by Parkerrush92 (talk • contribs) 05:19, 17 June 2017 (UTC)[reply]

An increase in the transmission of a transmitter. Received by the naturally present receptor. Is a neuron.

{true}

A received synaptic transmission is a neuron

{ }

Seratonin is naturally occuring and has a receptor.

Sertraline is not naturally occuring, and does not have a receptor.

Sertraline is a reuptake inhibitor.

Sertraline increases the prevalence of seratonin transmissions.

Seratonin is a transmittor, transmitted, in the form of a neuron.

pretty well stumped* Regards:Efficacy of antidepressant, treatment of, with, Sertraline:Deppression

Parkerrush92 (talk) 06:02, 17 June 2017 (UTC)[reply]

The current model of drug (chemical) treatment of symptoms is flawed.

The synaptic process is not being altered, in that, when drugs are processed, a neuron containing information is fired. This neuron CAN NOT BE modulated, created, or changed, by modern drug synthesis and metabolization.

The only drugs that are efficable in treatment, or those that dull senses, change experience, or lead to ignoring, or dulling, of symptoms. To say that a drug can affect mood is only true in a non chemical way, and that is the process in which treatment occurs, in proffesionaly managed trustworthy environments. Not placebo, because of different environmental variables, but not dissimilar in efficacy of treatment of symptoms.

If the brain knows, what symptoms are being treated, it CAN and DOES fire a neuron. This neuron CAN include relevant information and electronic signals. The brain CAN treat itself. I believe that the long term solution that a brain has for a person is often post-death. This can, and is often overridden, by something as simple as desire or belief. (in context of chronic, painful conditions.) *sad* *angry* *awareness*

This needs to be taught, so that the presence of mind can communicate with itself, and not throw itself in the garbage.

Pain management is true, when awareness of pain is gone. When awareness of pain is gone, most awareness is also gone. Treating pain, with pain killers, kills more than just pain. It interrupts signal processing, which affects all of the brain, except for the self managed regions, that are forced to respond, to the death and muting, of essential awareness processes, effectivley minimizing the brains ability to communicate and treat itself. *cancer*

The neurotransmission synaptic process appears to be a controlled environment, that is related to brain function. The brain uses this as a mechanism of protection, and communication. The unknown information inside of a neuron, is presumably related to experience. — Preceding unsigned comment added by Parkerrush92 (talk • contribs) 06:30, 17 June 2017 (UTC)[reply]