Potassium channels of the Kv7 family that mediate the non-inactivating M current regulate the excitability of many types of neurons in the central nervous system, including some in the hippocampus. We report here that individual interneurons from newborn rat hippocampi in long-term culture strongly express messenger RNA specific for Kv7.2 and Kv7.3 and, to a lesser extent, Kv7.5 channel subunits but not for the Kv7.4 subunit. An M-like current was electrophysiologically identified in two subpopulations of interneurons distinct in their spiking behaviour (regular or fast spiking). The M-channel enhancer retigabine reduced interneuronal excitability by constraining the number of action potentials generated during imposed depolarisations; this effect was inhibited by specific the M-channel blocking drugs. In paired synaptically connected interneuron-target cell recordings, anatomically localised applications of retigabine indicated that M channels were present in both the interneuron soma and its GABA-ergic inhibitory axon. We conclude that M-channel subunits and functional M channels are broadly expressed in hippocampal interneurons and their axons and are potentially capable of strongly regulating their firing properties.
Using a patch-clamp technique in the whole-cell configuration, we identified the potassium M-type current and estimated its contribution to the integral depolarization-induced potassium current evoked in cultured hippocampal inhibitory interneurons of the rat. With the help of immunocytochemical labeling, we checked the presence of the KCNQ-family channels responsible for generation of M current in these neurons. It was demonstrated that non-inactivated potassium channels and channels with slow kinetics play the main role in the processes of repolarization of the membrane of inhibitory interneurons. In all studied cells, a potassium current non-inactivated with time and possessing kinetic parameters close to those of the M current developed in response to depolarization. In all cells, positive immunocytochemical labeling with respect to KCNQ2 channels was observed; however, its intensity varied significantly from neuron to neuron. The level of suppression of non-inactivated potassium currents by a blocker of KCNQ channels, linopirdine, varied noticeably in different cells; therefore, the level of expression of these channels in the interneurons under study is probably considerably dissimilar. The reason for incomplete suppression of the M current is perhaps the involvement of other potassium channels (e.g., those of Kv1 family) in the formation of this current.
The expression and functioning of KCNQ potassium channels in the membranes of inhibitory interneurons of hippocampal culture and the involvement of these channels in the regulation of GABA-ergic synaptic transmission were investigated using a reverse transcription (RT) and polymerase chain reaction (PCR) for the single-cell technique (single-cell RT-PCR) and a patch-clamp technique in the "whole-cell" configuration. Expression of the genes of KCNQ2 and KCNQ3 α-subunits was revealed in all the GABA-ergic interneurons studied. A small level of the KCNQ5 subunit expression was detected in 38% of the cells. Activation of the somatic KCNQ channels of interneurons led to a shift in the resting potential toward more negative values, and also to the inability of these cells to generate spike series in response to prolonged depolarizing current injection. Functional KCNQ channels were also revealed in axons of inhibitory interneurons. Activation of these channels in the axons inhibited spike generation; this led to a decrease in GABA release from the terminals and, accordingly, to suppression of inhibitory synaptic responses in postsynaptic neurons.
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