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Departments of 1 Pharmacology and 2 Anesthesia, College of Medicine, University of Iowa, Iowa City 52242; and 3 Department of Veterans Affairs Medical Center, Iowa City, Iowa 52246
DiI-labeled colon sensory neurons were acutely dissociated from
S1 rat dorsal root ganglia (DRG) and studied using perforated whole
cell patch-clamp techniques. Forty-six percent (54/116) of labeled
sensory neurons responded to capsaicin
(10
8- 105
M) with an increase in inward current, which was a nonspecific cation
conductance. Responses to capsaicin applied by puffer ejection were
dependent on dose, with a half-maximal response at 4.9 × 107 M; bath application was
characterized by marked desensitization. Voltage-gated Na+
currents in 23 of 30 DRG cells exhibited both TTX-sensitive and TTX-resistant components. In these cells, capsaicin induced an inward
current in 11 of 17 cells tested. Of the cells containing only a
TTX-sensitive component, none of six cells tested was sensitive to
capsaicin. In all cells that responded to capsaicin with an increase in
inward current, capsaicin abolished voltage-gated Na+
currents (n = 21). Capsazepine
(106 M) significantly attenuated both
the increase in inward current and the reduction in Na+
currents. Na+ currents were not significantly altered by
adenosine, bradykinin, histamine, PGE2, or serotonin at
106 M and
105 M. These findings may have important
implications for understanding both the irritant and analgesic
properties of capsaicin.
visceral pain; bradykinin; prostaglandin E2; serotonin; tetrodotoxin
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