Nociceptive afferent activity alters the SI RA neuron response to mechanical skin stimulation

  • Whitsel B
  • Favorov O
  • Li Y
 et al. 
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Abstract

Procedures that reliably evoke cutaneous pain in humans (i.e., 5-7 s skin contact with a 47-51 °C probe, intradermal algogen injection) are shown to decrease the mean spike firing rate (MFR) and degree to which the rapidly adapting (RA) neurons in areas 3b/1 of squirrel monkey primary somatosensory cortex (SI) entrain to a 25-Hz stimulus to the receptive field center (RF(center)) when stimulus amplitude is "near-threshold" (i.e., 10-50 μm). In contrast, RA neuron MFR and entrainment are either unaffected or enhanced by 47-51 °C contact or intradermal algogen injection when the amplitude of 25-Hz stimulation is 100-200 μm (suprathreshold). The results are attributed to an "activity dependence" of γ-aminobutyric acid (GABA) action on the GABA(A) receptors of RA neurons. The nociceptive afferent drive triggered by skin contact with a 47-51 °C probe or intradermal algogen is proposed to activate nociresponsive neurons in area 3a which, via corticocortical connections, leads to the release of GABA in areas 3b/1. It is hypothesized that GABA is hyperpolarizing/inhibitory and suppresses stimulus-evoked RA neuron MFR and entrainment whenever RA neuron activity is low (as when the RF(center) stimulus is weak/near-threshold) but is depolarizing/excitatory and augments MFR and entrainment when RA neuron activity is high (when the stimulus is strong/suprathreshold).

Author-supplied keywords

  • bipolar GABA action
  • interareal interactions
  • mechanoresponsivity
  • pain-touch interaction
  • primary somatosensory cortex
  • vibrotactile frequency discrimination

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Authors

  • B. L. Whitsel

  • O. V. Favorov

  • Y. Li

  • J. Lee

  • P. M. Quibrera

  • M. Tommerdahl

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