Voltage-gated calcium channels act upstream of adenylyl cyclase Ac78C to promote timely initiation of dendrite regeneration.

Most neurons are not replaced after injury and thus possess robust intrinsic mechanisms for repair after damage. Axon injury triggers a calcium wave, and calcium and cAMP can augment axon regeneration. In comparison to axon regeneration, dendrite regeneration is poorly understood.

Dendrite regeneration mediates functional recovery after complete dendrite removal.

Unlike many cell types, neurons are not typically replaced if damaged. Therefore, regeneration of damaged cellular domains is critical for maintenance of neuronal function. While axon regeneration has been documented for several hundred years, it has only recently become possible to determine whether neurons respond to dendrite removal with regeneration.

The exocyst complex is required for developmental and regenerative neurite growth in vivo.

The exocyst complex is an important regulator of intracellular trafficking and tethers secretory vesicles to the plasma membrane. Understanding of its role in neuron outgrowth remains incomplete, and previous studies have come to different conclusions about its importance for axon and dendrite growth, particularly in vivo. To investigate exocyst function in vivo we used Drosophila sensory neurons as a model system.

Model validation for estimating taper microgroove deformation during total hip arthroplasty head-neck assembly.

Total hip arthroplasty (THA) failure and the need for revision surgery can result from fretting-corrosion damage of the head-neck modular taper junctions. Prior work has shown that implant geometry, such as microgrooves, influences damage on retrieved implants. Microgroove deformation within the modular taper junction occurs when the female head taper meets the male stem taper during THA surgical procedure.