Calcium signaling in skeletal muscle development, maintenance and regeneration.

Skeletal muscle-specific stem cells are pivotal for tissue development and regeneration. Muscle plasticity, inherent in these processes, is also essential for daily life activities. Great advances and efforts have been made in understanding the function of the skeletal muscle-dedicated stem cells, called muscle satellite cells, and the specific signaling mechanisms that activate them for recruitment in the repair of the injured muscle. Elucidating these signaling mechanisms may contribute to devising therapies for muscular injury or disease. Here we review the studies that have contributed to our understanding of how calcium signaling regulates skeletal muscle development, homeostasis and regeneration, with a focus on the calcium dynamics and calcium-dependent effectors that participate in these processes.

Spatiotemporal integration of developmental cues in neural development.

Nervous system development relies on the generation of neurons, their differentiation and establishment of synaptic connections. These events exhibit remarkable plasticity and are regulated by many developmental cues. Here, we review the mechanisms of three classes of these cues: morphogenetic proteins, electrical activity, and the environment. We focus on second messenger dynamics and their role as integrators of the action of diverse cues, enabling plasticity in the process of neural development.

The extent of myelin pathology differs following contusion and transection spinal cord injury.

Demyelination is a prominent feature of spinal cord injury (SCI) and is followed by incomplete remyelination, which may contribute to physiological impairment. Demyelination has been documented in several species including humans, but the extent of demyelination and its functional consequence remain unknown. In this report, we document and compare the extent of tissue pathology, white matter apoptosis, demyelination, and remyelination 2 months following injury in rat contusion and transection models of SCI. Moreover, we document and compare the macrophage response 3 and 14 days post contusion and transection SCI. Contusion injury resulted in widespread tissue pathology, white matter apoptosis, demyelination, incomplete remyelination, and robust macrophage response extending several millimeters cranial and caudal to the epicenter of injury. In contrast, transection injury resulted in focal tissue pathology with white matter apoptosis, demyelination, incomplete remyelination, and robust macrophage response at the epicenter of injury, and little pathologic features at a distance from the epicenter of injury, as indicated by the lack of apoptosis and demyelination. These data indicate for the first time that myelin pathology differs substantially following contusion and transection SCI.