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Journal of Neurophysiology, Vol 69, Issue 6 2129-2136, Copyright © 1993 by APS
ARTICLES |
G. Maccaferri, M. Mangoni, A. Lazzari and D. DiFrancesco
Dipartimento di Fisiologia e Biochimica Generali, Universita di Milano, Italy.
1. Voltage and current clamp recordings were performed on CA1 rat hippocampal pyramidal cells using the patch clamp technique on "in vitro" slice preparations. 2. Hyperpolarizations from a holding potential of -35 mV elicited activation of the hyperpolarization-activated current (Ih) starting at voltages near -50 mV. 3. Ih recorded in voltage clamp conditions was blocked by external caesium (5 mM). 4. Raising the external K concentration from 4.35 to 24.35 mM sensibly increased the slope of the current-voltage (I/V) curve. Decreasing the external Na concentration from 133.5 to 33.5 mM depressed Ih without grossly altering the I/V slope. 5. The Ih fully activated I/V relation measured in the range -140 to -45 mV was linear with an extrapolated reversal at -17.0 +/- -1.6 (SE) mV. The current activation curve comprised the range between about -50 and -140 mV with a half-maximal activation at about -98 mV. 6. Perfusion of unclamped neurons with Cs (2 mM) hyperpolarized their resting potential by 3.8 +/- 0.2 mV and decreased the membrane conductance, as expected if Ih were activated at rest. Firing caused by depolarizing current steps was prevented by Cs-induced hyperpolarization, and could be restored by returning the membrane voltage to resting level by constant current injection. 7. The Cd-insensitive (medium-duration) afterhyperpolarization (AHP) elicited by a train of action potentials at -60 mV had an amplitude of 3.9 +/- 0.3 mV and was nearly fully abolished by 2 mM Cs (82.7 +/- 7.4%). Cs removed the depolarizing part of the afterhyperpolarization as expected if Ih activation was responsible for this phase.(ABSTRACT TRUNCATED AT 250 WORDS)
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