A single channel recording showing the Kcv potassium channel activity in a cell-attached patch of HEK cell membrane transiently expressing the channel. The closed and opened levels are indicated by a dotted line preceded by C or O, respectively. The pipette holding potential is indicated at the right end of the trace. K+ concentration inside the pipette was 130 mM; K+ in bath solution was 100 mM.  

Measuring the reverse potential of HCN2 channel. HcN2 channel current activated by hyperpolarizing prepulse to -120mV, followed by a test pulse to potentials between -110 and -60 mV (top panel). Data were saved in .dat format and analyzed off-line using Mathlab software (The MathWorks, USA). Plotting the current at the beginning of the test pulse against the test pulse potential provides the instantaneous current–voltage relation. Fitting data with a linear regression yields the reversal potential of -21,88 mV (bottom panel), in agreement with the the experimental conditions (25 C°; [K+]in 130mM; [K+]out 30mM; [Na+]in 10mM; [Na+]out 110mM) and the published PNa/PK

– Biel, Martin, Christian Wahl-Schott, Stylianos Michalakis, and Xiangang Zong. 2009. “Hyperpolarization-Activated Cation Channels: From Genes to Function.” Physiological Reviews 89(3): 847–85.

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Voltage dependence of activation of hERG channel. Outward K+ current elicited by hERG channel transiently expressed in mammalian HEK293T cells (top panel). Cells were held at -80 mV and depolarized to voltages between -60 and +40 mV for 4 s, and then clamped to –50 mV for 6 s (centre panel). Data were saved in .abf format (Axon binary format v2.0) and analyzed off-line. Voltage-dependence of activation was obtained from plots of tail currents against voltage; fitting to the data with Boltzmann equation provides the half activation potential of -16,2 mV (bottom panel).

– Butler, Andrew et al. 2018. “Action Potential Clamp Characterization of the S631A HERG Mutation Associated with Short QT Syndrome.” Physiological reports 6(17)

ATP-evoked inward current of P2X2 receptor transiently expressed in mammalian HEK293T cells. The cell was held at -40mV under the whole-cell configuration. Scale bar 500 ms/1nA. ATP was delivered to the cell for ~ 1,5 s by means of an automated pinch valves prefusion system and then rapidly washed out (green and red bar respectively). The experiment was performed at RT.– Habermacher et al 2016 (eLife, 5:e11050).

Voltage-dependent activation of Nav1.5 sodium channel expressed in HEK293T cells. Representative whole-cell current traces recordedfrom a HEK-Nav1.5 cell,using the indicated pulse protocol. Data were recorded at 10KHz bandwidth (Sampling Rate: 80 KHz).Both pipette and membrane capacitance were compensated. Voltage errors were minimized using 80% series resistance compensation. Pipette was filled with a solution containing (in mM): 135 NaCl, 4 KCl, 1 CaCl2,2 MgCl2, 10 HEPES, 20 Glucose, PH 7.4. Bath solution contained (in mM): 5 NaCl, 140CsCl, 4 Mg-ATP, 2 MgCl2, 5 EGTA, 10 HEPES, PH 7.4. 

Whole-cell current-clamp recordings of a cortical neuron isolated from neonatal rat brains. After achieving the whole-cell configuration in VC mode, the amplifier was switched to the “true zero current mode” to measure the resting potential value. Afterwards, both the pipette neutralization and the bridge balance compensation were applied. The action potentials were finally recorded by injecting a series of current steps for 1 s (here is shown the most representative one) from the same holding potential of -70 mV. Data were acquired at 10 kHz SR and saved in .abf format.

– Data courtesy of Dr. A. Binda and Prof. I. Rivolta, School of Medicine and Surgery, University of Milano-Bicocca, Italy.

Mitochondrial permeability transition pore (mPTP) current recorded in excised patch clamp configuration. Ramp voltage protocol.

Mitochondria were isolated from neonatal mouse brain after ischemia reperfusion injury. Formation of mitoplast were induced by passive mitochondrial swelling without energy substrates. Recording was done in symmetric recording solution (150 mM KCl). Note the inhibition of mPTP channel activity after addition of Cyclosporin A (CsA). 

– Data courtesy of Dr. Maria Neginskaya, Dept. of Medicine, Albert Einstein College of Medicine, NYC