Background: Motoneurons with naturally elevated calcium binding protein content, such as
parvalbumin, are more resistant against injury. Furthermore, increase of intracellular calcium, which
plays a pivotal role in injury of neurons, could be moderated by elevating their calcium binding proteins.
Objective: To test whether by elevating parvalbumin content of motoneurons, activation of neighboring
microglial cells, a robust component of the inflammatory reaction after injury, could be influenced.
Methods: Mice overexpressing neuronal parvalbumin were derived and the spinal motoneurons were
challenged by cutting the sciatic nerve. At postoperative days 1, 4, 7, 14 and 21 the change of the
chemokine ligand 2 immunostaining in the motoneurons and the activation of microglial cells, measured
as alterations in CD11b immunostaining were determined. Calcium level of motoneurons was
tested electron microscopically at postoperative day 7.
Results: After axotomy, increased level of chemokine ligand 2 was detected in the lumbar motoneurons.
The staining intensity reached its maximum at day 7 and decayed faster in transgenic mice compared
to controls. Microglial activation around motoneurons attenuated faster in parvalbumin overexpressing
mice, too, but the decrease of microglial activation was delayed compared to the decline of the
chemokine ligand 2 signal. At the time when the microglial reaction peaked, no intracellular calcium
increase was detected in the motoneurons of transgenic mice, in contrast to the twofold increase in wild
Conclusion: Increased calcium buffering capacity, which augments resistance of motoneurons against
calcium-mediated injury, leads to earlier termination of motoneuronal emission of CCL2 followed by a
reduction of neighboring microglial activation after axotomy.