Journal of neurophysiology
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Temporal summation of heat pain during repetitive stimulation is dependent on C nociceptor activation of central N-methyl-d-aspartate (NMDA) receptor mechanisms. Moderate temporal summation is produced by sequential triangular ramps of stimulation that control skin temperature between heat pulses but do not elicit distinct first and second pain sensations. Dramatic summation of second pain is produced by repeated contact of the skin with a preheated thermode, but skin temperature between taps is not controlled by this procedure. ⋯ In contrast to heat stimulation, skin temperature did not recover between cold stimuli throughout ISIs of 3-8 s. Psychophysically, repetitive cold stimulation produced an aching pain sensation that progressed gradually and radiated beyond the site of stimulation. The magnitude of aching pain was well related to skin temperature and thus appeared to be established primarily by peripheral factors.
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During rhythmic voluntary oscillations of the foot, the excitability of the H-reflex in the Flexor Carpi Radialis (FCR) muscle of the resting prone forearm increases during the foot plantar-flexion and decreases during dorsiflexion. It is known that, when the two extremities are moved together, isodirectional (in-phase) coupling is the preferred form of movement association. Thus the above pattern of the H-reflex excitability modulation may favor the preferred coupling between the two limbs. ⋯ Simultaneously, the FCR H-reflex modulation advanced by that same amount with respect to the foot movement, thus remaining phase-locked to the EMG onsets. Similarly, when movement frequency was varied step-wise between 1.0 and 2.0 Hz, the foot movement was progressively delayed with respect to both the EMG onset (Sol and TA) and the FCR H-reflex modulation, so that the phase relation between the motor command to the foot and the H-modulation in the forearm remained constant. These results suggest that modulation of H-reflex in the forearm is tied to leg muscle contraction, rather than to foot kinematics, and point to a central, rather than kinesthetic, origin for the modulation.
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The contribution for the development of secondary mechanical hyperalgesia by peripheral mechanisms has not been fully elucidated. We have reevaluated the effects of local anesthetics on electrically evoked flare reaction and mechanical hyperalgesia in human skin. We applied 2% lidocaine via intradermal microdialysis fibers at a length of 10 cm for 110 min to the volar forearm to establish a narrow and stable "anesthetic strip." After 60 min of lidocaine perfusion, transdermal electrical stimulation (1 Hz, 50 mA) was applied at a distance of 1 cm from the microdialysis fibers for 30 min. ⋯ In contrast, allodynia (7.4 +/- 0.7 and 8.6 +/- 0.9 cm) and punctate hyperalgesia (7.6 +/- 0.7 and 8.6 +/- 0.9 cm) developed symmetrically on both sides of the anesthetic strip. Allodynia subsided 4 min after the end of the electrical stimulation. We conclude that the development of allodynia and punctate hyperalgesia in human skin is centrally mediated, whereas the axon reflex vasodilation is of peripheral origin.
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When studied in vitro, type I hair cells in amniote vestibular organs have a large, negatively activating K+ conductance. In type II hair cells, as in nonvestibular hair cells, outwardly rectifying K+ conductances are smaller and more positively activating. As a result, type I cells have more negative resting potentials and smaller input resistances than do type II cells; large inward currents fail to depolarize type I cells above -60 mV. ⋯ The Ca2+ current included an L-type component with relatively low sensitivity to dihydropyridine antagonists, consistent with the alpha subunit being CaV1.3 (alpha1D). Rat vestibular epithelia and ganglia were probed for L-type alpha-subunit expression with the reverse transcription-polymerase chain reaction. The epithelia expressed CaV1.3 and the ganglia expressed CaV1.2 (alpha1C).