Activity-dependent change in morphology of the glial tubular lattice of the crayfish medial giant nerve fiber

• Published in: Glia 2005-08, Vol.51 (2), p.121-131
• Main Authors: Beshay, Joseph E., Hahn, Paulette, Beshay, Victor E., Hargittai, Pal T., Lieberman, Edward M.
• Format: Article
• Language: English
• Subjects: Action Potentials - drug effects; Action Potentials - physiology; Animals; Astacoidea - physiology; Astacoidea - ultrastructure; axon; Axons - drug effects; Axons - physiology; Axons - ultrastructure; Biological and medical sciences; Body Water - metabolism; Cell Communication - drug effects; Cell Communication - physiology; Cell Membrane - drug effects; Cell Membrane - physiology; Cell Membrane - ultrastructure; Cell Size - drug effects; Electric Stimulation; electron microscopy; Fundamental and applied biological sciences. Psychology; glia; Isolated neuron and nerve. Neuroglia; Lanthanum; Microscopy, Electron, Transmission; Nerve Fibers - drug effects; Nerve Fibers - physiology; Nerve Fibers - ultrastructure; Neuroglia - drug effects; Neuroglia - physiology; Neuroglia - ultrastructure; potassium; Potassium - metabolism; Potassium Channel Blockers - pharmacology; TEA; tubular lattice; Vertebrates: nervous system and sense organs; Water-Electrolyte Balance - physiology
• ISSN: 0894-1491; 1098-1136
• DOI: 10.1002/glia.20192

An evaluation of electron micrographs of stimulated nerve fibers used to investigate the effect of action potential generation on the structure–function relationship between axons and its associated glial cells revealed that what was at first thought to be stimulation‐induced damage to the glia was, in fact, limited to volume expansion and disaggregation of the glial tubular lattice. All other structures appeared well preserved and otherwise normal. Using a 4‐point subjective scale for evaluation by two investigators, 50‐Hz stimulation for 2 min was observed to cause a volume expansion and disaggregation of the tubular lattice. Quantitatively, the internal diameter of the stimulated tubular lattice increased 65% above the unstimulated control (50.96 ± 2.09 nm and 30.81 ± 0.87 nm, respectively, P ≤ 0.001). Stimulation had its greatest effect on tubular lattice volume and organization in the adaxonal glial layer and a decreasing effect as distance from the giant axon increased. These effects are reversible since the tubular lattice diameter and degree of disaggregation preserved 10 min after the cessation of stimulation were not found to be different from their unstimulated paired controls. Axons injected with TEA, a voltage‐gated potassium channel blocker, prevented stimulation‐induced volume expansion and disaggregation of tubular lattice structure. These results are consistent with an active uptake of K+ with obligated water or, alternatively, hyperosmotic K+ uptake and a fixation‐induced increase in water permeation. Either mechanism of K+ uptake would result in tubular lattice volume expansion and disaggregation and suggests that the tubular lattice serves a larger role than a simple trans‐glial diffusion pathway. © 2005 Wiley‐Liss, Inc.