TY - JOUR
T1 - Potassium channel blockade induces action potential generation in guinea-pig airway vagal afferent neurones
AU - McAlexander, M. Allen
AU - Undem, Bradley J.
N1 - Funding Information:
This work was supported by funds from the National Institutes of Health, USA.
PY - 2000/1/14
Y1 - 2000/1/14
N2 - Electrophysiological studies of vagal sensory nerves with cell bodies in the nodose ganglion and mechanically sensitive receptive fields in the guinea-pig trachea/bronchus, were performed. Exposure of the mechanically sensitive receptive fields to 4-aminopyridine (100 μM-1 mM) caused pronounced action potential discharge in all fibres studied. Action potential generation was also produced by α-dendrotoxin, and in a subset of fibres, by barium. By contrast, neither iberiotoxin, tetraethyl ammonium, glybenclamide, BDS-II, nor apamin caused action potential generation in the vagal afferent nerve fibres. Tetramethylrhodamine dextran was instilled into the trachea to retrogradely label cell bodies within the nodose ganglion. In these cells, 4-aminopyridine caused a large depolarization of the resting membrane potential, concomitant with an increase in input impedance. The data suggest 4-aminopyridine- and α-dendrotoxin-sensitive ion channels within the airway afferent nerve membrane hold the resting membrane potential below the threshold for action potential generation. Mechanisms that lead to an inhibition of these channels will likely lead to an increase in excitability of the airway afferent neurones. Copyright (C) 2000 Elsevier Science B.V.
AB - Electrophysiological studies of vagal sensory nerves with cell bodies in the nodose ganglion and mechanically sensitive receptive fields in the guinea-pig trachea/bronchus, were performed. Exposure of the mechanically sensitive receptive fields to 4-aminopyridine (100 μM-1 mM) caused pronounced action potential discharge in all fibres studied. Action potential generation was also produced by α-dendrotoxin, and in a subset of fibres, by barium. By contrast, neither iberiotoxin, tetraethyl ammonium, glybenclamide, BDS-II, nor apamin caused action potential generation in the vagal afferent nerve fibres. Tetramethylrhodamine dextran was instilled into the trachea to retrogradely label cell bodies within the nodose ganglion. In these cells, 4-aminopyridine caused a large depolarization of the resting membrane potential, concomitant with an increase in input impedance. The data suggest 4-aminopyridine- and α-dendrotoxin-sensitive ion channels within the airway afferent nerve membrane hold the resting membrane potential below the threshold for action potential generation. Mechanisms that lead to an inhibition of these channels will likely lead to an increase in excitability of the airway afferent neurones. Copyright (C) 2000 Elsevier Science B.V.
KW - Airway
KW - Potassium channels
KW - Sensory nerves
KW - Vagus
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U2 - 10.1016/S0165-1838(99)00075-2
DO - 10.1016/S0165-1838(99)00075-2
M3 - Article
C2 - 10789695
AN - SCOPUS:0033977353
SN - 0165-1838
VL - 78
SP - 158
EP - 164
JO - Journal of the Autonomic Nervous System
JF - Journal of the Autonomic Nervous System
IS - 2-3
ER -