Uptake of locally applied deoxyglucose, glucose and lactate by axons and Schwann cells of rat vagus nerve

Vega, C., Martiel, J.-L., Drouhault, D., Burckhart, M.-F. and Coles, J. A. (2003) Uptake of locally applied deoxyglucose, glucose and lactate by axons and Schwann cells of rat vagus nerve. Journal of Physiology, 546(2), pp. 551-564. (doi: 10.1113/jphysiol.2002.029751)

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Publisher's URL: http://dx.doi.org/10.1113/jphysiol.2002.029751

Abstract

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. <sup>14</sup>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-<sup>14</sup>C]D-glucose (<sup>*</sup>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<sup>2</sup> s<sup>−1</sup> (± S.E.M., <i>n</i>= 16). Applications of <sup>*</sup>DG were repeated in the presence of the gap junction blocker, carbenoxolone (100 μM). 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<sup>2</sup> s<sup>−1</sup>, <i>n</i> = 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 % (<i>n</i> = 9) of the uptake of <sup>*</sup>DG was into Schwann cells. This suggests that there was transfer of metabolic substrate from Schwann cells to axons. Local application of [<sup>14</sup>C]glucose or [<sup>14</sup>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.

Item Type:Articles
Status:Published
Refereed:Yes
Glasgow Author(s) Enlighten ID:Coles, Dr Jonathan
Authors: Vega, C., Martiel, J.-L., Drouhault, D., Burckhart, M.-F., and Coles, J. A.
College/School:College of Medical Veterinary and Life Sciences > School of Infection & Immunity
Journal Name:Journal of Physiology
Publisher:Wiley
ISSN:0022-3751
ISSN (Online):1469-7793

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