AboutNeuron TypesElectrophysiology PropertiesArticlesFAQsData/APIGet Involved

Article: Modulation of Ca(2+)-activated K+ currents and Ca(2+)-dependent action potentials by exocytosis in goldfish bipolar cell terminals.

Full Text (publisher's website) ; Article Metadata ; Article Data (extracted)
Palmer MJ
J. Physiol. (Lond.), 2006

Table 2. Properties of membrane currents evoked by step depolarizations to −10 mV with potassium gluconate-containing intracellular solution, in the presence of picrotoxin (50 μm)

Control Nifedipine
Data were obtained from 17 control terminals and nine terminals in the presence of the L-type Ca2+ channel antagonist nifedipine (100 μm; three terminals were recorded from in both conditions). Step depolarizations in control conditions evoked an initial inward ICa followed rapidly by net outward current, which exhibited a biphasic profile. The degree of outward current inactivation during the first ∼25 ms was variable between recordings (no inactivation, n= 6; partial inactivation, n= 9; complete inactivation, n= 2). Nifedipine inhibited ICa and both the rapidly activated component and a slowly developing component of the outward current (IK(Ca)).
Peak inward current (pA) −112 ± 11  −13 ± 3 
Outward current at 3 ms (pA) 109 ± 10  4 ± 3
Outward current at 25 ms (pA)  76 ± 10 35 ± 9
Outward current at 200 ms (pA) 120 ± 12 37 ± 8
Outward current at 1 s (pA) 176 ± 20  41 ± 13

Report miscurated data

Inferred neuron-electrophysiology data values

Neuron Type Neuron Description Ephys Prop Extracted Value Standardized Value Content Source