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Received April 11, 2004
Revised April 26, 2004
Accepted after revision May 24, 2004
1 Dept. of Pharmacology & Exp. Therapeutics, Universit of Maryland, School of Medicine
2 Dept. of Pharmacology & Exp. Therapeutics, University of Maryland, School of Medicine
* To whom correspondence should be addressed. E-mail: dweinrei{at}umaryland.edu.
Bradykinin (BK) is an inflammatory mediator that can excite and sensitize primary afferent neurones. The nature of the ionic channels underlying the excitatory actions of BK is still incompletely understood. Using whole-cell patch-clamp recording from acutely dissociated nodose ganglion neurones (NGNs) we have examined the ionic mechanism responsible for BK's excitatory effect. Bath-applied BK (0.1 µM) depolarized the membrane potential (29 ± 3.1 mV, n=7), evoked action potentials, and induced an inward ionic current (IBK) with two distinctive membrane conductances (gm). Initially, gm decreased; the ionic current associated with this gm had an estimated reversal potential (Erev) value of -87 ± 1.1 mV (n=26), a value close to EK+ (-89 mV). Subsequently, gm increased; the ionic current associated with this gm had an estimated Erev of 49 ± 4.3 mV (n=23). When the second component was isolated from the first component, by replacing [K+]o with Cs+, Erev was 20 ± 4.7 mV (n=10). Replacing [NaCl]o with NMDG-Cl or choline-Cl, or reducing [Ca2+]o did not significantly diminish IBK. After replacing [NaCl]o with Na-isethionate, Erev for the second component shifted to 56 ± 8.8 mV (n=4), a value close to the ECl- (66 mV). The second component was inhibited by intracellular BAPTA or by bath application of niflumic acid (100 µM), a Ca2+-activated Cl- channel blocker. These results suggest that the first and second components of IBK are produced by a decrease in K+ conductance and an increase in Ca2+-activated Cl- conductance, respectively. The BK-evoked Cl- conductance in NGNs may be the first demonstration of an inflammatory mediator exciting primary afferents via an anion channel.
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