Nociceptive Afferent Activity Alters the SI RA Neuron Response to Mechanical Skin Stimulation

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...

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Published in:Cerebral cortex (New York, N.Y. 1991) Vol. 20; no. 12; pp. 2900 - 2915
Main Authors: Whitsel, B.L., Favorov, O.V., Li, Y., Lee, J., Quibrera, P.M., Tommerdahl, M.
Format: Journal Article
Language:English
Published: United States Oxford University Press 01-12-2010
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Summary: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 (RFcenter) 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 GABAA 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 RFcenter 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).
Bibliography:ark:/67375/HXZ-8R1X7FHQ-Z
Current address: Research Engineering Laboratory, Memorial Sloan-Kettering Cancer Center, New York, NY 10065, USA
istex:23C17AB8F0EBC930098E5285F56D473F19DBE8AE
ObjectType-Article-1
SourceType-Scholarly Journals-1
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content type line 23
ISSN:1047-3211
1460-2199
DOI:10.1093/cercor/bhq039