No abstract

We have studied the axonal projection patterns of commissural interneurons (CINs) in the neonatal rat spinal cord. Some CINs are integral components of the neuronal networks in the vertebrate spinal cord that generate locomotor activity. By using differential retrograde labeling protocols with fluorescent dextran amines, we show that CINs with ascending axons (ascending CINs, or aCINs) and CINs with descending axons (descending CINs, or dCINs) constitute largely different populations. We show that aCINs and dCINs occupy partially overlapping domains in the transverse plane. The aCINs are located at the dorsal margin, within the dorsal horn, centrally within the intermediate zone, and in the medial region of the ventral horn, whereas the dCINs are located predominantly among the ventral and central aCINs and in smaller numbers within the dorsal horn. The labeled aCINs and dCINs project for at least one and a half segment rostrally or caudally and are present in roughly equal numbers. We also demonstrate the presence of a third, smaller population of CINs whose axons bifurcate to project for at least one and a half segment both rostrally and caudally (adCINs). The adCINs are located predominantly among the central and ventral groups of aCINs and dCINs. Finally, we demonstrate the presence of CINs with axons projecting for fewer than one and a half segment in either direction. These "short-range CINs" are intermingled with the aCINs, dCINs, and adCINs. Our results provide an anatomical framework for further electrophysiological studies aimed at identifying the CINs that participate in the mammalian locomotor central pattern generator.

High-intensity exercise was a strong and independent marker of life-threatening VA in AC patients, independent of exercise duration. AC patients could be advised to restrict their exercise intensity.

Following contraction of the heart, efficient relaxation (diastole) is essential for refilling the ventricles with blood. This review describes how ventricular relaxation is controlled by Ca(2+) homeostasis in cardiac muscle cells and how alterations in Ca(2+) cycling affect diastolic function in the normal and failing heart. These discussions illustrate that the diastolic phase is not simply a period of rest but rather involves highly regulated and dynamic Ca(2+) fluxes.