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Uptake of locally applied deoxyglucose, glucose and lactate by axons and schwann cells of rat vagus nerve
Author(s) -
Véga Céline,
Martiel JeanLouis,
Drouhault Delphine,
Burckhart MarieFrance,
Coles Jonathan A.
Publication year - 2003
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.2002.029751
Subject(s) - carbenoxolone , gap junction , chemistry , vagus nerve , biophysics , compartment (ship) , substrate (aquarium) , schwann cell , diffusion , steady state (chemistry) , anatomy , endocrinology , biology , biochemistry , intracellular , stimulation , physics , ecology , oceanography , geology , thermodynamics
We asked whether, in a steady state, neurons and glial cells both take up glucose sufficient for their energy requirements, or whether glial cells take up a disproportionate amount and transfer metabolic substrate to neurons. A desheathed rat vagus nerve was held crossways in a laminar flow perfusion chamber and stimulated at 2 Hz. 14 C‐labelled substrate was applied from a micropipette for 5 min over a < 0.6 mm band of the surface of the nerve. After 10‐55 min incubation, the nerve was lyophilized and the longitudinal distribution of radioactivity measured. When the weakly metabolizable analogue of glucose, 2‐deoxy‐[U‐ 14 C] d ‐glucose (*DG), was applied, the profiles of the radioactivity broadened with time, reaching distances several times the mean length of the Schwann cells (0.32 mm; most of the Schwann cells are non‐myelinating). The profiles were well fitted by curves calculated for diffusion in a single compartment, the mean diffusion coefficient being 463 ± 34 μm 2 s −1 (± s.e.m ., n = 16). Applications of *DG were repeated in the presence of the gap junction blocker, carbenoxolone (100 μ m ). The profiles were now narrower and better fitted with two compartments. One compartment had a coefficient not significantly different from that in the absence of the gap junction blocker (axons), the other compartment had a coefficient of 204 ± 24 μm 2 s −1 , n = 4. Addition of the gap junction blocker 18‐α‐glycyrrhetinic acid, or blocking electrical activity with TTX, also reduced longitudinal diffusion. Ascribing the compartment in which diffusion was reduced by these treatments to non‐myelinating Schwann cells, we conclude that 78.0 ± 3.6 % ( n = 9) of the uptake of *DG was into Schwann cells. This suggests that there was transfer of metabolic substrate from Schwann cells to axons. Local application of [ 14 C]glucose or [ 14 C]lactate led to variable labelling along the length of the nerve, but with both substrates narrow peaks were often present at the application site; these were greatly reduced by subsequent treatment with amylase, a glycogen‐degrading enzyme.