The Discharge of Specific, Cold Fibres at High Temperatures

Abstract

STRUMPELL 1881 described neurological cases displaying specific anesthesia to cold and reported a very distinct heat sensation when the skin was touched by pieces of ice. It was less often that they found the opposite phenomenon i. e. that heating the skin produced a sensation of cold. In the following years these "paradoxical sensations" were much discussed (see LEHMANN 1892 and v. FREY 1895) and it was definitely established that the stimulation of single cold spots with heat above 45" C led t o a sensation of cold. The existence of a paradoxical cold sensation is thus rather generally accepted while the corresponding paradoxical heat sensation still is under debate. The problem of whether the warm receptors can be stimulated by rapid cooling will be treated by us in another paper in connection with the mode of action of the warm receptors. The purpose of the present study was to investigate how specific cold fibres of the cat's tongue react t o a rise in temperature of the surface of the tongue t o different levels. Methods.The preparation of fine strands of the lingual nerve of the cat as well as the recording of spikes from specific cold fibres has previously been described by ZOTTERMAN (1936). The stimulating devices for the teni-

Nociceptive sensations evoked from ‘spots’ in the skin by mild cooling and heating

“…However, the possibility that LTN arises from classically defined cold fibers and warm fibers cannot be ruled out, as the thresholds of fibers that express TRPM8 and TRPV3 fall within the range of putative cold and warm fibers. Support for involvement of cold fibers comes from their 'paradoxical' response to high temperatures (Dodt and Zotterman 1952;Long 1973;Campero et al 2001) and from the phenomenon of the heat grill illusion, or 'synthetic heat' (Green 1977;Green 2002;Fruhstorfer et al 2003). Whereas the high threshold [>50°C; (Long 1977)] and temporal irregularity of the paradoxical discharge rule out a role for cold fibers in encoding heat pain, evidence that repeated heating sensitizes cold fibers to heat and lowered the threshold of the paradoxical discharge (Dubner et al 1975;Long 1977) led to speculation that cold fibers may contribute to heat hyperalgesia (Dubner et al 1975;Price and Dubner 1977).…”

Ion channels involved in cold detection in mammals: TRP and non-TRP mechanisms

“…More recent evidence was provided for the expression of TRPM8 in C and thinly myelinated Aδ fibers that terminate in the superficial layers of the spinal dorsal horn (mostly lamina I), as well as for the substantial overlap between TRPM8 and TRPV1 (Takashima et al 2007;Dhaka et al 2008). The functional consequence of this overlap between TRPM8 and TRPV1 is not entirely understood, but it may underlie the phenomenon of paradoxical activation of low threshold cold receptors by noxious heat (Dodt and Zotterman 1952).…”

The Emerging Role of TRP Channels in Mechanisms of Temperature and Pain Sensation

“…Within the DRG and trigeminal ganglia, TRPV1 is most abundantly expressed in small diameter C-fibers that express CGRP, SP and IB4. It is also found within sensory fibers that innervate the viscera, urinary bladder and airways [17,42,43,76,93,139]. Consistent with the central projections of these neurons, TRPV1 immunoreactivity is localized to CNS regions such as the superficial laminae (I and II) of the dorsal horn of the spinal cord and nucleus of the solitary tract [50,139].…”

“…Two groups have studied the role of TRPV4 in mediating acute noxious heat detection and inflammatory thermal hyperalgesia by analyzing TRPV4-/-mice [81,138]. In the first study, acute noxious heat sensation of TRPV4-/-mice appears intact, with no significant difference compared to wildtype in escape latencies in hot plate (35)(36)(37)(38)(39)(40)(41)(42)(43)(44)(45)(46)(47)(48)(49)(50) o C) or radiant heat tests [138]. In this same study, TRPV4-/-mice display longer escape latencies from hot plate compared to wildtype following hindpaw injection of carrageenan, indicating that TRPV4 plays a role in mediating inflammation induced thermal hyperalgesia.…”