Pierre-Paul Van Bogaert

Kv2.1 and silent Kv subunits underlie the delayed rectifier K current in cultured small mouse DRG neurons

Silent voltage-gated K(+) (K(v)) subunits interact with K(v)2 subunits and primarily modulate the voltage dependence of inactivation of these heterotetrameric channels. Both K(v)2 and silent K(v) subunits are expressed in the mammalian nervous system, but little is known about their expression and function in sensory neurons. This study reports the presence of K(v)2.1, K(v)2.2, and silent subunit K(v)6.1, K(v)8.1, K(v)9.1, K(v)9.2, and K(v)9.3 mRNA in mouse dorsal root ganglia (DRG). Immunocytochemistry confirmed the protein expression of K(v)2.x and K(v)9.x subunits in cultured small DRG neurons. To investigate if K(v)2 and silent K(v) subunits are underlying the delayed rectifier K(+) current (I(K)) in these neurons, K(v)2-mediated currents were isolated by the extracellular application of rStromatoxin-1 (ScTx) or by the intracellular application of K(v)2 antibodies. Both ScTx- and anti-K(v)2.1-sensitive currents displayed two components in their voltage dependence of inactivation. Together, both components accounted for approximately two-thirds of I(K). A comparison with results obtained in heterologous expression systems suggests that one component reflects homotetrameric K(v)2.1 channels, whereas the other component represents heterotetrameric K(v)2.1/silent K(v) channels. These observations support a physiological role for silent K(v) subunits in small DRG neurons.

Alinidine modifies the pacemaker current in sheep Purkinje fibers

Abstract(1) The “specific bradycardic agent” alinidine reduces the slope of the diastolic depolarization in sinoatrial tissue and Purkinje fibers. In short Purkinje fibers of sheep, alinidine (28 μM) decreased the pacemaker current by a dual action. The voltage dependence ofif activation was shifted in the hyperpolarizing direction by 7.8±0.6 mV (n=18,p<0.001) and the conductance of the fully activated

Kv3 channels contribute to the delayed rectifier current in small cultured mouse dorsal root ganglion neurons

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The contribution of Kv2.2‐mediated currents decreases during the postnatal development of mouse dorsal root ganglion neurons

current was reduced to 73±2% (n=18,p<0.001) of its control value. These effects were reversible and dose-dependent. (2) Ionophoretic injections of alinidine caused reversible reductions of the diastolic depolarization rate and simultaneous transient hyperpolarizing shifts of theif activation range. (3) Some prolongation of the action potential duration was observed at 28 μM and more pronounced at higher concentration. This was presumably the consequence of a reduction by alinidine of outward repolarizing current carried by the background inward rectifier and plateau currentix. (4) The action of alinidine onif resulted in a slower activation of a reduced fraction of the pacemaker current at the maximal diastolic potential level. This explains the decrease of the diastolic depolarization rate observed in Purkinje fibers.

Endogenous guanidino compounds as uremic neurotoxins

Abstract1.Cardiac Purkinje fibers exposed to alkaline solutions (pH 8 to 9.5) show an increase in rate of diastolic depolarization, eventually resulting in induction of spontaneous activity or an increase of the spontaneous firing rate.2.The voltage-clamp analysis of the transmembrane currents in pH 9–9.5 shows: i) a shift in the depolarizing direction of the activation (s∞) and time constants (τs) curve of the

Intrinsic choroidal neurons in the human eye: projections, targets, and basic electrophysiological data

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