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This Article Full Text Full Text (PDF) All Versions of this Article: 102/1/424    most recent 90916.2008v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Google Scholar Articles by Greffrath, W. Articles by Treede, R.-D. PubMed PubMed Citation Articles by Greffrath, W. Articles by Treede, R.-D.

Heat-Induced Action Potential Discharges in Nociceptive Primary Sensory Neurons of Rats

¹Division of Neurophysiology, Center of Biomedicine and Medical Technology Mannheim, Medical Faculty Mannheim, Ruprecht-Karls-University Heidelberg, Mannheim; ²Institute of Physiology and Pathophysiology, Johannes Gutenberg University, Mainz, Germany; ³Nottingham University Hospitals Trust, Nottingham, United Kingdom; and ⁴Texas Tech University–Health Sciences Center, Paul L. Foster School of Medicine, El Paso, Texas

Submitted 15 August 2008; accepted in final form 10 May 2009

Although several transducer molecules for noxious stimuli have been identified, little is known about the transformation of the resulting generator currents into action potentials (APs). Therefore we investigated the transformation process for stepped noxious heat stimuli (42–47°C, 3-s duration) into membrane potential changes and subsequent AP discharges using the somata of acutely dissociated small dorsal root ganglion (DRG) neurons (diameter 32.5 µm) of adult rats as a model for their own peripheral terminals. Three types of heat-induced membrane potential changes were differentiated: type 1, heat-induced AP discharges (37% of the neurons); type 2, heat-induced membrane depolarization (40%); and type 3, responses not exceeding those of switching the superfusion (23%). Warming neurons from room temperature to 35°C increased their background conductance, nearly doubled the AP threshold current, and led to smaller and narrower APs. Adaptation of heat-induced AP discharges was seen in about half of the type 1 neurons. The remaining half displayed accelerating discharges to both heat stimuli and depolarizing current injection. Repeated heat stimulation induced marked suppression of AP discharges. Under rapid calcium buffering using BAPTA, repolarization of heat-induced APs stopped at a plateau potential slowly decreasing from +16.5 ± 2.9 to –2.2 ± 5.5 mV, resulting in no further AP discharges. This study demonstrates that heat-induced AP discharges can be elicited in the soma of a subgroup of DRG neurons. These discharges display suppression on repetitive stimulation, but either adaptation or sensitization during prolonged stimuli. AP threshold and AP shape during these discharges suggest temperature dependence of background conductance and repolarizing currents.