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Cerebral Cortex Advance Access originally published online on June 4, 2008
Cerebral Cortex 2009 19(2):349-366; doi:10.1093/cercor/bhn086
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© The Author 2008. Published by Oxford University Press. All rights reserved. For permissions, please e-mail: journals.permissions@oxfordjournals.org

Area 3a Neuron Response to Skin Nociceptor Afferent Drive

Barry L. Whitsel1,2, Oleg V. Favorov1, Yongbiao Li1,3, Miguel Quibrera2 and Mark Tommerdahl1

1 Department of Biomedical Engineering, 2 Department of Cell and Molecular Physiology, University of North Carolina, School of Medicine, Chapel Hill, NC 27599, USA

Address correspondence to B. L. Whitsel, PhD, 406A MacNider Building, CB#7545, University of North Carolina, School of Medicine, Chapel Hill, NC 27599-7545, USA. Email: bwhitsel{at}med.unc.edu.

Area 3a neurons are identified that respond weakly or not at all to skin contact with a 25–38 °C probe, but vigorously to skin contact with the probe at ≥49 °C. Maximal rate of spike firing associated with 1- to 7-s contact at ≥49 °C occurs 1-2 s after probe removal from the skin. The activity evoked by 5-s contact with the probe at 51 °C remains above-background for ~20 s after probe retraction. After 1-s contact at 55–56 °C activity remains above-background for ~4 s. Magnitude of spike firing associated with 5-s contact increases linearly as probe temperature is increased from 49–51 °C. Intradermal capsaicin injection elicits a larger (~2.5x) and longer-lasting (100x) increase in area 3a neuron firing rate than 5-s contact at 51 °C. Area 3a neurons exhibit enhanced or novel responsivity to 25–38 °C contact for a prolonged time after intradermal injection of capsaicin or {alpha}, β methylene adenosine triphosphate. Their 1) delayed and persisting increase in spike firing in response to contact at ≥49 °C, 2) vigorous and prolonged response to intradermal capsaicin, and 3) enhanced and frequently novel response to 25–38 °C contact following intradermal algogen injection or noxious skin heating suggest that the area 3a neurons identified in this study contribute to second pain and mechanical hyperalgesia/allodynia.

Key Words: hyperalgesia • neurophysiology • nociception • pain • primary somatosensory cortex

3 Present address: Research Engineering Laboratory, Memorial Sloan-Kettering Cancer Center, New York, NY 10065, USA.


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