TY - JOUR
T1 - Hyperpolarization-activated current (I(h)) in primary auditory neurons
AU - Chen, Chu
N1 - Funding Information:
Thanks to Dr. Richard P. Bobbin for his support and guidance, and J. Campbell for her technical help. This work was supported in part by a Deafness Research Foundation grant, Kam's fund for Hearing Research, and the Louisiana Lions Eye Foundation.
PY - 1997/8
Y1 - 1997/8
N2 - A hyperpolarization-activated current (termed I(h)) is believed to provide a pacemaker depolarization in sinoatrial node cells and in some central and peripheral neurons. In the present study, we examined if such an inward cation current exists in primary auditory neurons using the whole- cell patch-clamp technique. A large inward, non-inactivating current was seen during hyperpolarizing steps negative to the resting potential. A depolarizing sag occurred during hyperpolarizing current injection, and upon termination of the current injection there was an overshoot, or a rebound firing. A low concentration of Cs+, but not Ba2+, reversibly blocked the inward current and depolarizing sag. The activation of the current showed voltage dependence with half-activation occurring at -101 ± 1 mV. The time course of I(h) activation was fitted by double exponential function and was voltage-dependent (time constants: τ1 and τ2=480 and 3125 ms at -100 mV, and 66 and 404 ms at -160 mV). The reversal potential of the current was -36 mV measured from tail currents. The conductance of the current was decreased in Na+-free solution, and increased in high K+ solution. Increases in the levels of intracellular cAMP or cGMP enhanced the current. The results suggest that there exists a hyperpolarization-activated inward cation current in mammalian primary auditory neurons. This current may provide a depolarizing current during the membrane hyperpolarization following each firing of the primary auditory nerve.
AB - A hyperpolarization-activated current (termed I(h)) is believed to provide a pacemaker depolarization in sinoatrial node cells and in some central and peripheral neurons. In the present study, we examined if such an inward cation current exists in primary auditory neurons using the whole- cell patch-clamp technique. A large inward, non-inactivating current was seen during hyperpolarizing steps negative to the resting potential. A depolarizing sag occurred during hyperpolarizing current injection, and upon termination of the current injection there was an overshoot, or a rebound firing. A low concentration of Cs+, but not Ba2+, reversibly blocked the inward current and depolarizing sag. The activation of the current showed voltage dependence with half-activation occurring at -101 ± 1 mV. The time course of I(h) activation was fitted by double exponential function and was voltage-dependent (time constants: τ1 and τ2=480 and 3125 ms at -100 mV, and 66 and 404 ms at -160 mV). The reversal potential of the current was -36 mV measured from tail currents. The conductance of the current was decreased in Na+-free solution, and increased in high K+ solution. Increases in the levels of intracellular cAMP or cGMP enhanced the current. The results suggest that there exists a hyperpolarization-activated inward cation current in mammalian primary auditory neurons. This current may provide a depolarizing current during the membrane hyperpolarization following each firing of the primary auditory nerve.
KW - Current-clamp
KW - Hyperpolarization-activated current
KW - Inward rectifying channel
KW - Primary auditory nerve
KW - Spiral ganglion neuron
KW - Voltage- clamp
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U2 - 10.1016/S0378-5955(97)00078-6
DO - 10.1016/S0378-5955(97)00078-6
M3 - Article
C2 - 9282900
AN - SCOPUS:0030858344
SN - 0378-5955
VL - 110
SP - 179
EP - 190
JO - Hearing Research
JF - Hearing Research
IS - 1-2
ER -