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Published on: November 11, 2017
Loose-patch recordings reveal differential Kv7-dependent effects on spontaneous excitatory activity in control and
Ella Marie Nissen1, Timo Kirschstein1,2, Astrid Bertsche3
1Oscar Langendorff Institute of Physiology, University Medical Center Rostock, Rostock, Germany.
Introduction:
The non-inactivating potassium channels Kv7.2 and Kv7.3 contribute to the neuronal resting membrane potential and regulate neuronal excitability. Previous studies have indicated a transcriptional downregulation of these channels in temporal lobe epilepsy, both in patients and in the pilocarpine-induced animal model. However, the functional consequences of this alteration for synaptic activity have not yet been fully elucidated.
Methods:
To investigate the role of Kv7 channels in epileptic tissue, we used the pilocarpine model of temporal lobe epilepsy. We performed loose-patch clamp recordings from the perisomatic region of CA1 pyramidal neurons and triggered putative spontaneous excitatory postsynaptic currents (EPSCs) with 5 μM gabazine and 6 mM extracellular K+. The effects of the selective Kv7 channel blocker XE991 on EPSC frequency, amplitude, and waveform kinetics (rise time, half-width, decay time) were compared between control and epileptic tissue.
Results:
XE991 produced opposing, non-significant within-cell trends in EPSC frequency (decrease in control vs. increase in epileptic tissue), while the absolute EPSC frequency under XE991 differed significantly between groups across all responsive cells (p = 0.006). Moreover, XE991 was associated with a trend toward larger EPSC amplitudes and prolonged waveform kinetics, an effect that was more consistently observed in control tissue than in epileptic tissue.
Discussion/Conclusion:
These findings demonstrate differential effects of Kv7 channel blockade on spontaneous EPSC frequency and waveform kinetics in epileptic versus control CA1 neurons. The enhanced frequency response, combined with less consistent effects on EPSC waveform duration and amplitude in epileptic tissue, suggests altered Kv7 channel function in the epileptic CA1 region. Together with previous evidence of persistent transcriptional down-regulation of Kv7 channels in the same pilocarpine model, these results support the hypothesis that Kv7 channel dysfunction contributes to network hyperexcitability in temporal lobe epilepsy.
