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Lack of Regulation by Intracellular Ca 2+ of the Hyper Polarization‐Activated Cation Current in Rat Thalamic Neurones
Author(s) -
Budde Thomas,
Biella Gerardo,
Munsch Thomas,
Pape HansChristian
Publication year - 1997
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.1469-7793.1997.079bi.x
Subject(s) - intracellular , depolarization , biophysics , stimulation , chemistry , hyperpolarization (physics) , reversal potential , patch clamp , neuroscience , electrophysiology , stereochemistry , biology , biochemistry , nuclear magnetic resonance spectroscopy
1 The regulation of the hyperpolarization‐activated cation current, I h , in thalamocortical neurones by intracellular calcium ions has been implemented in a number of mathematical models on the waxing and waning behaviour of synchronized rhythmic activity in thalamocortical circuits. In the present study, the Ca 2+ dependence of I h in thalamocortical neurones was experimentally investigated by combining Ca 2+ imaging and patch‐clamp techniques in the ventrobasal thalamic complex (VB) in vitro.2 Properties of I h were analysed before and during rhythmic stimulation of Ca 2+ entry by trains of depolarizing voltage pulses. Despite a significant increase in intracellular Ca 2+ concentration ([Ca 2+ ] i ) from resting levels of 74 ± 23 nM to 251 ± 78 nM upon rhythmic stimulation, significant differences in the voltage dependence of I h activation did not occur (half‐maximal activation at −86.4 ± l.3 mV vs. −85.2 ± 2.9 mV; slope of the activation curve, 11.2 ± 2.4 mV vs. 12.5 ± 2.5 mV). Recording of I h with predefined values of [Ca 2+ ] i (13.2 nM or 10.01 μm in the patch pipette) revealed no significant differences in the activation curve or the fully activated I–V relationship of I h . 3 In comparison, stimulation of the intracellular cyclic adenosine monophosphate (cAMP) pathway induced a significantly positive shift in I h voltage dependence of +5.1 ± l.9 mV, with no alteration in the fully activated I–V relationship. 4 These data argue against a direct regulation of I h by intracellular Ca 2+ , and particularly do not support a primary role of Ca 2+ ‐dependent modulation of the I h channels in the waxing and waning of sleep spindle oscillations in thalamocortical neurones.