A fully implantable pacemaker for the mouse: from battery to wireless power.

Animal models have become a popular platform for the investigation of the molecular and systemic mechanisms of pathological cardiovascular physiology. Chronic pacing studies with implantable pacemakers in large animals have led to useful models of heart failure and atrial fibrillation. Unfortunately, molecular and genetic studies in these large animal models are often prohibitively expensive or not available.

Repolarization changes underlying long-term cardiac memory due to right ventricular pacing: noninvasive mapping with electrocardiographic imaging.

Background: Cardiac memory refers to the observation that altered cardiac electrical activation results in repolarization changes that persist after the restoration of a normal activation pattern. Animal studies, however, have yielded disparate conclusions, both regarding the spatial pattern of repolarization changes in cardiac memory and the underlying mechanisms. The present study was undertaken to produce 3-dimensional images of the repolarization changes underlying long-term cardiac memory in humans.

Characterization of a novel, dominant negative KCNJ2 mutation associated with Andersen-Tawil syndrome.

Andersen-Tawil syndrome is characterized by periodic paralysis, ventricular ectopy, and dysmorphic features. Approximately 60% of patients exhibit loss-of-function mutations in KCNJ2, which encodes the inwardly rectifying K(+) channel pore forming subunit Kir2.1.

Mechanisms linking short- and long-term electrical remodeling in the heart...is it a stretch?

Ion channels play a central role in the normal electro-mechanical functioning of the heart and are implicated in a variety of disease processes. In response to electrical or mechanical perturbations, cardiac myocytes exhibit remarkable changes in the expression and/or the function of sarcolemmal ion channels, a process that is broadly described as electrical remodeling. This remodeling has beneficial, as well as adverse, effects on myocardial function, including increased risk of fatal arrhythmias.

Investigating the safety factor at an invertebrate neuromuscular junction.

Fidelity of synaptic transmission is essential at the neuromuscular junction (NMJ). To ensure that transmission does not fail, vertebrate motoneurons often release more neurotransmitter than is required for muscle contraction. This safety factor allows some loss of synaptic function without failure of muscle contraction.

Preferential localization of glutamate receptors opposite sites of high presynaptic release.

Background: The localization of glutamate receptors is essential for the formation and plasticity of excitatory synapses. These receptors cluster opposite neurotransmitter release sites of glutamatergic neurons, but these release sites have heterogeneous structural and functional properties. At the Drosophila neuromuscular junction, receptors expressed in a single postsynaptic cell are confronted with an array of hundreds of apposed active zones.

Differential localization of glutamate receptor subunits at the Drosophila neuromuscular junction.

The subunit composition of postsynaptic neurotransmitter receptors is a key determinant of synaptic physiology. Two glutamate receptor subunits, Drosophila glutamate receptor IIA (DGluRIIA) and DGluRIIB, are expressed at the Drosophila neuromuscular junction and are redundant for viability, yet differ in their physiological properties. We now identify a third glutamate receptor subunit at the Drosophila neuromuscular junction, DGluRIII, which is essential for viability.