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The voltage‐dependent conductances of rat neocortical layer I neurons
Author(s) -
Budde Thomas,
White John A.
Publication year - 1998
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1046/j.1460-9568.1998.00242.x
Subject(s) - chemistry , patch clamp , biophysics , tetraethylammonium , time constant , membrane potential , tetrodotoxin , 4 aminopyridine , cardiac transient outward potassium current , potassium channel , depolarization , potassium , biochemistry , biology , receptor , organic chemistry , electrical engineering , engineering
Whole cell patch‐clamp techniques were used to study voltage‐dependent sodium (Na + ), calcium (Ca 2+ ), and potassium (K + ) conductances in acutely isolated neurons from cortical layer I of adult rats. Layer I cells were identified by means of γ‐aminobutyric acid (GABA) immunocytochemistry. Positive stainings for the Ca 2+ ‐binding protein calretinin in a subset of cells, indicated the presence of Cajal–Retzius (C‐R) cells. All investigated cells displayed a rather homogeneous profile of voltage‐dependent membrane currents. A fast Na + current activated at about −45 mV, was half‐maximal steady‐state inactivated at −66.6 mV, and recovery from inactivation followed a two‐exponential process (τ 1 = 8.4 ms and τ 2 = 858.8 ms). Na + currents declined rapidly with two voltage‐dependent time constants, reaching baseline current after some tens of milliseconds. In a subset of cells (< 50%) a constant current level of < 65 pA remained at the end of a 90 ms step. A transient outward current (I fast ) activated ≈–40 mV, declined rapidly with a voltage‐insensitive time constant (τ≈ 350 ms) and was relatively insensitive to tetraethylammonium (TEA, 20 m m ). I fast was separated into two components based on their sensitivity to 4‐aminopyridine (4‐AP): one was blocked by low concentrations (40 μ m ) and a second by high concentrations (6 m m ). After elimination of I fast by a conditioning prepulse (50 ms to −50 mV), a slow K + current (I KV ) could be studied in isolation. I KV was only moderately affected by 4‐AP (6 m m ), while TEA (20 m m ) blocked most (> 80%) of the current. I KV activated at about −40 mV, declined monoexponentially in a voltage‐dependent manner (τ≈ 850 ms at −30 mV), and revealed an incomplete steady‐state inactivation. In addition to I fast and I KV , indications of a Ca 2+ ‐dependent outward current component were found. When Na + currents, I fast , and I KV were blocked by tetrodotoxin (TTX, 1 μ m ), 4‐AP (6 m m ) and TEA (20 m m ) an inward current carried by Ca 2+ was found. Ca 2+ currents activated at depolarized potentials at about −30 mV, were completely blocked by 50 μ m cadmium (Cd 2+ ), were sensitive to verapamil (≈ 40% block by 10 μ m ), and were not affected by nickel (50 μ m ). During current clamp recordings, isolated layer I neurons displayed fast spiking behaviour with short action potentials (≈ 2 ms, measured at half maximal amplitude) of relative small amplitude (≈ 83 mV, measured from the action potential threshold).