Itch, medically referred to as pruritus, is a nocifensive neural sensation most everyone has experienced. It can be induced by touches only microns in length, like the legs of an insect or the spines of a plant (Twycross, 2003). Unimpressive as they seem, brushing and scratching responses itch are important to our health. Without these evolved defences, we would be increasingly susceptible to a range of consequences – from the bite of a landing mosquito to severe contact dermatitis (Oaklander, 2012).
Cutaneous itch – the warning – comes to be when a pruritogen is detected by epidermal peripheral nerve endings with pruritogenic receptors. This generates a pathway of afferent action potentials down a system of specialized nerve cells (Twycross, 2003). The facial Gasserian ganglion, depicted in Figure 1, is one such neuronal system (Purves, Augustine, and Fitzpatrick, 2001).
The electrical signal travels down the peripheral nerve axons, and into the receptive field of unmyelinated nociceptors (Twycross, 2003). Not to be confused with pain-transmitting nociceptors (anatomically the same but functionally different), itch-mediating nociceptors have a slower average conduction velocity of 0.5 m/s and wider receptive fields of 85 mm diameter (Purves, Augustine, and Fitzpatrick, 2001).
Dorsal root ganglia are next to receive the signal, bringing it through spinal nerves to the thalamus and finally the cerebral cortex where itch is consciously perceived (Purves, Augustine, and Fitzpatrick, 2001). An efferent response signal for the body to physically relieve the itch is sent back via the peripheral system (Mochizuki, Papoiu, and Yosipovitch, 2014).
Unfortunately, this sequence is not always completed in time to successfully remove a pruritogenic threat; skin may then be exposed to chemical mediators causing more serious conditions (Oaklander, 2012).
Toxicodendron radicans is one example. Commonly referred to as poison ivy, this plant belongs to a genus notorious for its allergenic sap. Its active ingredient, represented in Figure 2, is the compound pentadecylcatechol which diffuses into the dermis upon contact. Its metabolism produces protein complexes that are unfamiliar to the immune system; in response, T-cells attack the complexes, also damaging the surrounding epidermal tissue and aggravating pruritogenic neurons (Gladman, 2014).
In this way, touching poison ivy results in a condition called contact dermatitis, characterized by a blistering rash and constantly itchy, inflamed skin – an allergenic itch (Oaklander, 2012 and Gladman, 2014).
Ironically, there is nothing in the sap of poison ivy that would be truly harmful to mammals, if not for the immune response induced in 85-90% of the North American population (Gladman, 2014) . In this way, Toxicodendron interacts with the mammalian nervous system via a neurological false alarm – a simple but effective strategy for defence.
Works Cited
Gladman, A.C., 2014. Toxicodendron Dermatitis: Poison Ivy, Oak, and Sumac, Wilderness & Environmental Medicine, 17(2), pp.120 – 128.
Kaufmann A.M., and Patel, M., 2001. Your Complete Guide to Trigeminal Neuralgia. University of Manitoba, unpublished.
Mochizuki, H., Papoiu, A.D.P., and Yosipovitch, G., 2014. Brain Processing of Itch and Scratching. In: E. Carstens and T. Akiyama, ed. 2014. Itch: Mechanisms and Treatment. Boca Raton: CRC Press. Ch.23.
Oaklander, A.L., 2012. Common Neuropathic Itch Syndromes, Acta Derm Venereol, 92, pp.118-125.
Purves D., Augustine G.J., and Fitzpatrick D., 2001. Neuroscience. 2nd ed. Sunderland: Sinauer Associates.
Twycross, R., 2003. Itch: scratching more than the surface, Q J Med, 96, pp.2-26.