Abstract

In many clinical pain syndromes, painful sensations are greatly amplified so that normally innocuous sensations, such as light touch or warmth, are perceived as pain. Presently available drugs are ineffective in controlling such pain in most patients and abolish the pain in only few. Why do they fail? These drugs were developed to target neurons that transmit nociceptive ('pain') information. However, glia have recently been recognized as powerful modulators of nociception, and could hold the key to the control of clinical pain and present a new target for drug discovery. This review examines the evidence for glial regulation of nociception and pharmacological approaches that might successfully control glially driven clinical pain syndromes.

Author affiliations

1. Department of Psychology and the Center for Neuroscience, University of Colorado at Boulder, Boulder, Colorado 80309-0345, USA.

Correspondence to: Linda R. Watkins¹ Email: lwatkins@psych.colorado.edu.