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J Neurophysiol. 1996 Aug;76(2):668-82.

Layer I neurons of the rat neocortex. II. Voltage-dependent outward currents.

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  • 1Neurobiology Research Center, University of Alabama at Birmingham 35294, USA.

Abstract

1. Whole cell patch-clamp techniques, combined with direct visualization of neurons, were used to study voltage-dependent potassium currents in layer 1 neurons and layer II/III pyramidal cells. 2. In the presence of tetrodotoxin, step depolarizations evoked an outward current. This current had a complex waveform and appeared to be a composite of early and late components. The early peak of the composite K+ outward current was larger in layer I neurons. 3. In both layer I and pyramidal cells, the composite outward K+ current could be separated into two components based on kinetic and pharmacological properties. The early component was termed I(A) because it was a transient outward current activating rapidly and then decaying. I(A) was more sensitive to blocking by 4-aminopyridine (4-AP) than tetraethylammonium (TEA). The second component, termed the delayed rectifier or I(DR), activated relatively slowly and did not decay significantly during a 200-ms test pulse. I(DR) was insensitive to blocking by 4-AP at concentrations up to 4 mM and blocked by > 60% by 40-60 mM TEA. 4. I(A) kinetics were examined in the presence of 40-60 mM TEA. Under these conditions, I(A) began to activate between -40 and -30 mV. Half-maximal activation occurred around 0 mV. In both layer I and pyramidal cells, the half-inactivation potential (Vh-inact) was around or more positive than -50 mV. At -60 mV, > 70% of I(A) conductance was available. I(A) decayed along a single exponential time course with a time constant of approximately 15 ms. This decay showed little voltage dependence. 5. In both layer I and pyramidal cells, I(DR) was studied in the presence of 4 mM 4-AP to block I(A) and in saline containing 0.2 mM Ca2+ and 3.6 mM Mg2+ to reduce contributions from Ca2+-dependent K+ currents. Under these conditions, I(DR) began to activate at -35 to -25 mV with Vh-act of 3.6 +/- 4.5 mV (mean +/- SD). The 10-90% rise time of I(DR) was 15 ms at 30 mV. At 2.2 ms after the onset of the command potential to +30 mV, I(DR) could reach a significant amplitude (approximately 1.5 nA in layer I neurons and 2.2 nA in pyramidal cells depending on the cell size). When long test pulses (> or = 1,000 ms) were used, a decay time constant approximately 800 ms at +40 mV was observed. In both layer I and pyramidal cells, steady state inactivation of I(DR) was minimal. 6. These results indicate that I(A) and I(DR) are the two major hyperpolarizing currents in layer I and pyramidal cells. The kinetics and pharmacological properties of I(A) and I(DR) were not significantly different in fast-spiking layer I neurons and regular-spiking layer II/III pyramidal cells. The relatively positive activation threshold (more than or equal to -40 mV) of both I(A) and I(DR) suggest that they do not play a role in neuronal behavior below action potential (AP) threshold and that their properties are more suitable to repolarize AP. The greater density of I(A) in layer I neurons appears responsible for fast spike generation.

PMID:
8871190
[PubMed - indexed for MEDLINE]
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