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The Section about the comparison with C fibers is huge... maybe someone should try and shorten it a bit? Or at least make it more readable (paragraphs, etc) —Preceding unsigned comment added by 89.152.108.25 (talk) 13:21, 29 May 2008 (UTC)[reply]
Hello.
I am a member of WikiProject Medicine, a Wikipedia wide project that maintains and improves articles that fall under the scope of medicine. Since your article is already under has our tag, I have now reassessed it to make sure if is in the right WikiProject. Upon reassessment of the article, I'd like to make a few points, as shown below:
Reassess article with class and importance factors
Reassessed tags for correct placements
Added neuro task force
Leave a message on my talk page if you have any questions. I'm glad this article could fall within our scope, and I hope to see it grow large! Many thanks! Renaissancee(talk)22:46, 4 June 2009 (UTC)[reply]
Conclusions in the literature remain largely mixed pertaining to the interaction between chemical stimuli and Aδ fibers. However, there is evidence that chemically noxious stimuli, such as capsaicin or certain acids, activate Aδ fibers to elicit pain associated with the potential for tissue damage. It has been suggested that acid-sensing ion channels (ASICS) play a role in acid-stimulated nociception involving Aδ fibers.[1] Capsaicin, the primary component of hot peppers which yields the experience of spice, may stimulate a common transducer, vanilloid receptor (VR1), in Aδ fibers.[2]
Have removed the above from page as it is at odds with info on Group C fibers which is also stated in ref given - See para starting Unmyelinated nerve fibers. Couldn't find anything relevant to ASICS in ref given.--Iztwoz (talk) 20:54, 9 December 2017 (UTC)[reply]
Aδ fibers respond to temperature on both the noxiously cold and hot ends of the spectrum. For both extremes, there exists a temperature threshold at which receptors begin to respond. Two main classes divide Aδ fibers: Type I and Type II. Type I receptors have higher heat thresholds then Type II. Thus, Type II Aδ fibers likely act as a first response to dangerously high temperatures.[3] Mechanistically, temperatures above 43°C activate a receptor associated with Aδ fibers called transient receptor potential vanilloid subfamily, member 1 (TRPV1) which subsequently depolarizes the neuron.[4] This depolarization is transmitted to the spinal cord where axons of Aδ fibers terminate on second-order neurons in the dorsal horn. These neurons relay the nociceptive signal to the brain (specifically the thalamus and the brainstem) for further processing.[5] At the cold end of the spectrum, it is clear that a significant proportion of Aδ fibers plays a role in perceiving cold temperatures, but the mechanism and related receptors are currently up for debate. Temperatures at or below ~ 15°C are cited as the cold threshold for painful stimuli. However, the threshold for Aδ fibers specifically seems to be lower (less than 0°C).[6]
Have removed above - wrong info on hot and cold; wrong info on two types of A delta; what is an axon of an A delta fiber? --Iztwoz (talk) 23:22, 9 December 2017 (UTC)[reply]
