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The Invagination of Excess Surface Area by Shrinking Neurons

C. E. Morris ^*, J. A. Wang ^* and V. S. Markin 

^* Neuroscience, Ottawa Health Research Institute, Ottawa Hospital, Ottawa, Ontario, Canada; and Department of Anesthesiology/Pain Management, University of Texas Southwestern Medical Center, Dallas, Texas

Correspondence: Address reprint requests to C. E. Morris, Neuroscience, Ottawa Health Research Institute, Ottawa Hospital, 725 Parkdale Ave., Ottawa, Ontario, Canada K1Y 4E9. Tel.: 613-798-5555 ext. 18608; Fax: 613-761-5330; E-mail: cmorris{at}ohri.ca.

Over most of their surface, neurons are surrounded by a narrow extracellular gap across which they make adhesive cell-cell contacts. Thus constrained, how do they regulate their geometry when osmotically perturbed? Specifically, are there any interesting consequences of local osmosis in such conditions? Using confocal imaging of shrinking neurons in culture, we observe water exiting into the cell-substratum gap. This water efflux generates a hydrostatic pressure that, at discrete (low adhesion) sites, causes the neuron's excess plasma membrane to invaginate, thus compensating for shrinkage with a pseudo-intracellular volume. To identify the minimal requirements of the process, a compartment/flux model was constructed. It comprises, essentially, a large liposome adhering in a labyrinthine fashion to a substratum. The model predicts that invaginations form at the cell-substratum interface under the influence of local osmosis, provided that adhesion across the gap is neither too tight nor too loose. Local osmosis in the central nervous system, in contrast to epithelia, is usually considered a mishap, not a physiological opportunity. We postulate, however, that local osmotic forces acting in conjunction with confined extracellular spaces could be harnessed in service of surface area, shape, and volume regulation when intense neural activity alters a neuron's osmotic balance.