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Hyperpolarization‐activated cationic currents ( I h ) in neurones of the trigeminal mesencephalic nucleus of the rat
Author(s) -
Khakh Baljit S.,
Henderson Graeme
Publication year - 1998
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1111/j.1469-7793.1998.00695.x
Subject(s) - hyperpolarization (physics) , membrane potential , chemistry , biophysics , reversal potential , extracellular , patch clamp , receptor , biochemistry , stereochemistry , biology , nuclear magnetic resonance spectroscopy
1 We studied the voltage‐dependent current activated by membrane hyperpolarization in sensory proprioceptive trigeminal mesencephalic nucleus (MNV) neurones. 2 Membrane hyperpolarization (from ‐62 to ‐132 mV in 10 mV steps) activated slowly activating and non‐inactivating inward currents. The hyperpolarization‐activated currents could be described by activation curves with a half‐maximal activation potential ( V ½ ) of ‐93 mV, slope ( k ) of 8.4 mV, and maximally activated currents (I max ) of around 1 nA. The reversal potential of the hyperpolarization‐activated currents was ‐57 mV. 3 Extracellular Cs + blocked hyperpolarization‐activated currents rapidly and reversibly in a concentration‐dependent manner with an IC 50 of 100 μM and Hill slope of 0.8. ZD7288 (1 μM; 4‐( N ‐ethyl‐ N ‐phenylamino)‐1,2‐dimethyl‐6‐(methylamino) pyridinium chloride), the compound developed as an inhibitor of the cardiac hyperpolarization‐activated current (I f ), also blocked the hyperpolarization‐activated currents in MNV neurones. Extracellular Ba 2+ (1 mM) did not affect hyperpolarization‐activated currents. We tested whether the hyperpolarization‐activated currents contribute to the somatic membrane properties of MNV neurones by performing some experiments using current‐clamp recording. In such experiments application of Cs + (1 mM) produced no effect on neuronal resting membrane potentials. 4 During the course of our experiments we noticed that activating ATP‐gated non‐selective cation channels (P2X receptors) caused an inhibition of I h associated with a V ½ shift of 10 mV in the hyperpolarizing direction. This P2X receptor‐mediated inhibition of I h was blocked in recordings made with the rapid calcium chelator BAPTA (11 mM) in the pipette solution. 5 We conclude that the current activated by membrane hyperpolarization in MNV neurones is I h on the basis of its similarity to I h observed in other neuronal preparations. Activation of I h can account for the anomalous time‐dependent inward rectification that has previously been described in MNV neurones.