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Surges R, Freiman TM, Feuerstein TJ: Input resistance is voltage dependent due to activation of Ih channels in rat CA1 pyramidal cells. J Neurosci Res. 2004 May 15;76(4):475-80.
The contribution of the hyperpolarization-activated cation current (I (h)) to input resistance (R (N)) and resting potential (RP) was investigated during whole-cell patch-clamp recordings in CA1 pyramidal cells of rat hippocampal slices. In current-clamp mode, R (N) was determined at different membrane potentials. R (N) decreased with increasing hyperpolarization, from about 260 Momega to 140 Momega at potentials of about -60 mV and -110 mV, respectively. Both the potential of half-maximal reduction of R (N) and the potential of half-maximal I (h) activation (determined in voltage-clamp mode) were approximately -90 mV. The analysis of the voltage sag indicative of I (h) activation revealed a preferential activity of I (h) channels in a voltage range between -70 and -95 mV. ZD7288 (50 microM), a specific I (h) blocker, led to a hyperpolarization by about 4.8 mV, increased R (N) by approximately 45% within a potential range between -65 and -80 mV, and abolished the voltage dependence of R (N). Gabapentin (GBP, 100 microM), an I (h) channel agonist, led to a depolarization by about 2.4 mV and reduced R (N) by about 20% within a potential range between -65 and -80 mV. In conclusion, our data show that R (N) is voltage dependent due to I (h) channel activation and that I (h) channels are preferentially active at voltages between -70 and -95 mV. Furthermore, we demonstrated that R (N) can be modulated by antiepileptic drugs such as GBP, which may partly explain its antiepileptic effect as due to decreasing the sensitivity to excitatory input. |
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