Evidence for two different heat transduction mechanisms in nociceptive primary afferents innervating monkey skin.

Abstract

1. Mechano-and heat-sensitive A fibre nociceptors (AMHs) and C fibre nociceptors (CMHs) in hairy skin (forty-six AMHs and twenty-one CMHs) and in glabrous skin (fifty-nine AMHs and ten CMHs) of anaesthetized monkeys were tested with a 30 s, 53°C heat stimulus, delivered by a laser thermal stimulator (0a1 s rise time, 7-5 mm diameter). 2. Two types of heat response were observed in hairy skin AMHs. Type I AMHs had a peak discharge towards the end of the stimulus, response latencies to heat of up to several seconds, a median heat threshold greater than 53°C, and a mean conduction velocity of 25 m s-' (n = 33). Type II AMHs had a peak discharge within 1-3 s, a mean response latency of 120 ms, a median heat threshold of 46°C, and a mean conduction velocity of 15 m s-' (n = 13). Type I AMH fibres were sensitized to heat, whereas heat responses of type II AMHs were suppressed following the intense heat stimulus. 3. In glabrous skin, only type I AMHs were found. The absence of type II AMHs is consistent with the absence of first pain to heat in glabrous skin. 4. C fibre nociceptors in hairy skin had a peak discharge near stimulus onset, a mean response latency of 100 ms and a median heat threshold of 41°C. Heat responses of CMHs in glabrous skin were not significantly different from those in hairy skin. 5. Only type II AMHs had response latencies that were short enough to explain first pain to heat. Heat thresholds of type II AMHs were significantly higher than those of CMHs. 6. These results suggest two different heat transduction mechanisms in nociceptive afferents.For one, heat energy is quickly transduced into action potentials, and the peak discharge is reached soon after stimulus onset. For the other, the transduction of heat is distinctly slower, and the peak discharge occurs near the end of the stimulus. Chemically mediated sensitization may be involved in the second transduction mechanism.

Response of C fibre nociceptors in the anaesthetized monkey to heat stimuli: correlation with pain threshold in humans.

“…The correlation of pain sensation with CMH discharge rate extends into the suprathreshold range: both magnitude of heat pain and discharge rate of human CMHs were found to increase with increasing ramp rate (Yarnitsky, Simone, Dotson, Cline & Ochoa, 1992). We assumed that the contribution of type II A fibre mechano-heat-sensitive nociceptors (Meyer, Campbell & Raja, 1994) to pain threshold can be ignored because their median threshold in monkey hairy skin is 46°C (Treede, Meyer, Raja & Campbell, 1995). We also considered the possible role of spatial summation.…”

Nociceptors: the sensors of the pain pathway

“…Under normal conditions, the activity in only a subset of heat-responsive fibers correlates to the degree of pain perceived (C-MH, A-MH type I, A-MH type II; Tables 1 and 2). A-fibers (A-MH Type II innervating hairy skin) responding to temperatures slightly cooler than the perceptual pain threshold for heat are proposed to mediate first pain in humans (55). These fibers rapidly activate, adapt during prolonged heat stimulation, fatigue between heat stimuli, and are sensitive to capsaicin (55-57), a selective agonist of the mammalian heat-activated nonselective cation (NSC) channel transient receptor potential VI (TRPV1) (58) ( Table 3).…”

Gamma-Band Oscillations in the Primary Somatosensory Cortex—A Direct and Obligatory Correlate of Subjective Pain Intensity

“…Most interestingly, the fact that GBOs constitute the only laser-induced EEG response which predicts the amount of perceived pain regardless of the saliency content of the stimulus, indicates that these neural activities originating from SI contribute directly to the emergence of a painful percept in response to nociceptive input. The early latency (86-328 ms) and short-lasting duration (242 ms) of laser-induced GBOs indicates that they are mediated by rapidly adapting type II A-fiber mechano-heat nociceptors responsible for the sensation of first pain (Treede et al, 1995). However, the possibility that GBOs reflect cortical activity that is specific for the processing of somatosensory input, but not specific for the processing of nociceptive input should not be dismissed.…”