Contribution of the Kv3.1 potassium channel to high‐frequency firing in mouse auditory neurones

摘要: 1. Using a combination of patch-clamp, in situ hybridization and computer simulation techniques, we have analysed the contribution potassium channels to ability subset mouse auditory neurones fire at high frequencies. 2. Voltage-clamp recordings from principal medial nucleus trapezoid body (MNTB) revealed low-threshold dendrotoxin (DTX)-sensitive current (ILT) high-threshold DTX-insensitive (IHT). 3. IHT displayed rapid activation deactivation kinetics, was selectively blocked by low concentration tetraethylammonium (TEA; 1 mM). 4. The physiological pharmacological properties very closely matched those Shaw family channel Kv3.1 stably expressed CHO cell line. 5. An mRNA probe corresponding C-terminus strongly labelled MNTB neurones, suggesting that this is these neurones. 6. TEA did not alter follow stimulation up 200 Hz, but specifically reduced their higher frequency impulses. 7. A simulation, using model which an outward with kinetics voltage dependence incorporated, also confirmed Kv3.1- like essential for cells respond sustained train high-frequency stimuli. 8. We conclude contributes lock firing inputs.