Talk:TRPV1

Clinical Significance: Central Nervous System

Current text suggests that antagonizing TRPV1 might have therapeutic value in preventing seizures, however this reasoning only becomes clear with close reading of Gibson et al. which demonstrated LTD only on excitatory synapses onto inhibitory interneurons. Text should be updated to reflect this. Additionally, a perusal of the literature on 12-HPETE the active eicosanoid identified in Gibson et al. yields the finding that LTD can be induced at CA3 to CA1 pyramidal cells with the compound (Feinmark et al 2003. J. Neuroscience. 12-Lipoxygenase Metabolites of Arachidonic Acid Mediate Metabotropic Glutamate Receptor-Dependent Long-Term Depression at Hippocampal CA3-CA1 Synapses). Thus any claims of therapeutic value of agonizing or antagonizing TRPV1 for the purposes of treating or preventing temporal lobe epilepsy are at the least highly dubious.

Suggest inclusion of Feinmark et al. and note controversy, and removal of potential therapeutic treatments targeting TRPV1 in the CNS. WLMorgan (talk) 15:27, 22 May 2010 (UTC)

Location?

Where are these receptors located? There is no heading for location and no description of where these receptors are found. The only clue is the declaration of "significance" in the Central Nervous System and the pheripheral nervous system, which is too vague. If these are found only on certain neuron types or branches that would also be nice to know. Stephen Charles Thompson (talk) 11:57, 2 January 2013 (UTC)

Neurotransmitter?

If there is no neurotransmitter, and activation of the receptor is caused only by other classes of triggers, that would be good to know. Stephen Charles Thompson (talk) 12:01, 2 January 2013 (UTC)

Hacking?

This section is theoretical and not at all germane to a basic discussion of the receptor. The first paragraph in particular is much to narrow in it's scope - that's the kind of thing that belongs in a journal article. Jgcimino (talk) 20:08, 27 March 2013 (UTC)

Fatty acid conjugates (cleanup needed)

There are a number of grammatical mistakes in the writing of this section. Because I have not researched the material covered in this section, specifically related to endocannabanoids, I decided not to fix them. Xkit (talk) 16:35, 24 March 2015 (UTC)

Recent addition

I have removed the following text:

text

9-Hydroxyoctadecadienoic acid (i.e. both the 9(S)-hydroxyoctadecadienoic acid (HODE) and 9(R)-HODE Stereoisomers) and 13-Hydroxyoctadecadienoic acid (i.e. both the 13(S)-HODE and 13(R)-HODE stereoisomers) along with their respective keto derivatives, 9-oxoODE and 13-oxoODE, stimulate TRPV1-dependent responses in rodent neurons, rodent and human bronchial epithelial cells, and in model cells made to express rodent or human TRPV1; this stimulation appears due to a direct interaction of these agents on TRPV1 although reports disagree on the potencies of these oxidized linoleic acid metabolites (OXLAM) with, for example, the most potent OXLAM, 9(S)-HODE, requiring at least 10 micromoles/liter or a more physiological concentration of 10 nanomoles/liter to activate TRPV1 in rodent neurons. Nonetheless, this effect of the OXLAMS gains importance in studies that find that they act through TRPV1 to mediate the perception of pain induced by heat, UV light, and inflammation in rodents and to mediate severe bronchial injury in mouse models of allergic airway disease. The studies propose that the OXLAMS-TRPV1 circuit contributes to pain perception as well as severe asthma disease in humans. References

for the following reasons:

• Wikipedia is not a journal. The material is way too detailed for a general encyclopedia intended for a wide audience.
• The focus of this article is about TRPV1, not ligands of TRPV1.
• The added material is not well organized and misplaced. We already have well established sections on function, ligands, and clinical significance. The above text mixes all three up and should be split up and place in the appropriate sections.
• Per WP:CITEVAR, editors should not change a previously established citation format. The above uses a different citation format. Given a PMID. the Wikipedia template filling tool can quickly produce a full citation that can be copied and pasted into this article which is compatible with the current citation format.
• Secondary sources are generally preferred, especially when supporting medical claims (see WP:MEDRS). The above sources are all primary. Boghog (talk) 19:16, 8 September 2015 (UTC)

External links modified

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Merger suggestion

The article Discovery and development of TRPV1 antagonists is a more than four year old university assignment. I think that it would be appropriate to merge its content here.81.236.207.188 (talk) 21:54, 20 August 2016 (UTC)

• Support – There was a previous discussion here and here and I think the general consensus at that time was not to merge these types of articles because there was a concern that these extensive Discovery and development articles would overwhelm whatever they were merged with (i.e., WP:UNDUE). Given that the main interest in TRPV1 is that it is a drug target, I don't think this is a concern in this case. Sorry for reverting the initial merger, but I think given the previous discussion, it is better to revisit to get consensus first. Boghog (talk) 17:52, 21 August 2016 (UTC)

• Oppose There is a set of these "Discovery and development of..." pages listed together under Drug design#Case Studies which make a nice teaching resource. I don't think there is any particular need to merge this page with the page for the receptor target, and it might lead to the other pages being merged with their respective targets too. I wouldn't want to see useful material trimmed out at a later stage because it was felt to put undue weight on that aspect on the page for the receptor target. Meodipt (talk) 09:18, 23 August 2016 (UTC)
• Oppose. I think separate articles work best - combining the two would result in either a loss of useful information or a single page overwhelmed with information. -- Ed (Edgar181) 23:02, 12 November 2016 (UTC)