Spinal cord ultrastructure and the distribution of aquaporin-4 in a rodent model of post-traumatic syringomyelia


Syringomyelia is characterised by an imbalance between fluid inflow and outflow. The exact mechanisms involved in this fluid accumulation, however, are unknown. Previous studies conducted by our laboratory have implicated aquaporin-4, a membranous water channel protein, in post-traumatic syringomyelia (PTS).


Transmission electron microscopy was used to investigate in detail the anatomical components involved in fluid exchange, as well as the localisation and expression of aquaporin-4 in a rodent model of PTS. Ultrathin (60 – 70 nm) spinal cord sections at the level of the syrinx were counterstained for structural anatomy (cohort: PTS, n = 3; control, n = 2) or immunogold labelled in triplicate for aquaporin-4 expression (cohort: PTS, n = 3; control, n = 2).


Several abnormalities in spinal cord tissue were identified from animals with syringomyelia, including enlarged perivascular spaces, extracellular oedema, cell death and loss of tissue integrity, demyelination, and a disruption of the blood spinal cord barrier, with increased pinocytotic transport across vascular walls. In addition, preliminary results suggest that concentric localisation of aquaporin-4 to astrocytic endfeet was unique to capillaries, with only amorphous expression found around arterioles and venules. Interestingly, discrete differences in the cellular organisation of aquaporin-4 at perivascular regions were not found between animals with syringomyelia and healthy controls.

Discussion and Conclusions

These initial findings suggest that syringomyelia does not change the distribution or result in the mislocalisation of aquaporin-4. However, it is likely to be associated with a change in the number of water-channel proteins present. This will be analysed further to establish whether there are changes in aquaporin-4 expression at specific fluid interfaces. The results of this study will elucidate whether aquaporin-4 expression corresponds to the anatomical changes observed in syringomyelia and may provide precise targets for future treatment therapies.