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The mechanical and biochemical parameters of connective tissue components of several organs in rats, e.g. skin, tail tendons and aorta, have been compared. Organ samples have been analyzed at various ages allowing investigation of the changes during maturation and senescence. The age dependent changes in the various organs were quite similar. The parameters indicating strength and elasticity, e.g. ultimate load, ultimate strength, ultimate strain, modulus of elasticity and rate of load increase, rose sharply during the maturation process and decreased during senescence. These values correlated with changes in insoluble collagen but not with those in elastin or glycosaminoglycans as shown in earlier experiments. The relevance of mechanical models to explain age-dependent changes as compared to descriptive correlations between mechanical and biochemical data is discussed.

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The location of the human nociceptive area(s) near the Sylvian fissure is still controversial in spite of evidence from imaging and evoked potential studies that noxious heat stimuli activate somatosensory areas in that region. Some studies have suggested the secondary somatosensory cortex (SII) on the upper bank of the Sylvian fissure posterior to the central sulcus, others the anterior insula or parietal area 7b. In this study, we applied dipole source analysis techniques to laser-evoked potentials (LEPs) that were recorded from subdural grid electrodes in three patients. As a functional marker, auditory-evoked potentials (AEPs) with a generator on the opposite bank of the Sylvian fissure were recorded from the same electrodes. The LEP global field power (GFP), a measure of spatial variance, showed a first peak at about 150 ms latency, corresponding to the latency of the N1 recorded from the scalp. In contrast to scalp recordings, the amplitude of the first GFP peak recorded from the grid was larger than the second peak (P2). This finding suggests that the generator of N1, but not that of later LEP components, was close to the subdural grids. When a regional source was fitted to the first GFP peak, its location was within the frontoparietal operculum in all patients. On average, the LEP source was 13 mm anterior, 6 mm superior, and 2 mm medial of the AEP source. This relative location also suggests a source within the frontoparietal operculum overlying the insula. At the latency of the first GFP peak, source orientation pointed inward, suggesting a generator within the inner vertical surface of the operculum. Somatotopy was assessed in one patient and was consistent with that of the projection area of the presumed nociceptive thalamic nucleus posterior part of the ventromedial nucleus, but differed from that of SII. These findings suggest that the nociceptive area in human parasylvian cortex that is activated most rapidly by noxious heat pulses may be separate from the tactile SII area.

Radiant heat is often used to study nociception in vivo. We now used infrared radiation generated by a diode laser stimulator (wavelength 980 nm) to investigate transduction mechanisms for noxious heat stimuli in acutely dissociated dorsal root ganglion (DRG) neurons of rats in vitro. The laser stimulator offered the unique opportunity to test whether the same stimuli also elicit pain sensations in humans. A specific heat-induced current (I(heat)) was elicited in six of 13 small DRG neurons (diameter < or =30 microm) tested in the whole-cell configuration of the patch-clamp mode. Current responses in the seven heat-insensitive neurons were within the range explainable by the temperature dependence of the recording setup. I(heat) was characterized by: (1) non-linearity of its amplitude during a suprathreshold heat ramp as well as with stimuli of increasing intensity with an estimated threshold of 42 +/- 1 degrees C; (2) fast rise time and even faster decay time (t(1/2) = 96.5 +/- 5.9 and 27.7 +/- 1.5 ms, respectively); and (3) rate dependence of its induction. All three heat-sensitive neurons tested were also sensitive to capsaicin. The mean threshold for the induction of I(heat) was 2.8 +/- 0.3 J mm(-2). The threshold for the induction of action potentials by depolarizing current pulses was significantly reduced after laser stimulation, suggesting a sensitization at the transformation stage. No such change was seen in heat-insensitive neurons that underwent the same heat stimuli. The same diode laser elicited pain sensations and laser-evoked potentials in human subjects. No significant differences were seen between the pain thresholds in hairy and in glabrous skin, probably due to the deep penetration of this laser radiation. The mean pain threshold for stimuli > or =200 ms in humans was 2.5 +/- 0.2 J mm(-2) (n = 11), and did not differ from the thresholds for the induction of I(heat) in vitro. Our results indicate that I(heat) in primary sensory neurons can be activated by infrared laser pulses that are painful in humans.

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