Elsevier

Neuroscience

Volume 8, Issue 3, March 1983, Pages 449-457
Neuroscience

The corticopontine projection: Axotomy-induced loss of high affinity l-glutamate and d-aspartate uptake, but not of γ-aminobutyrate uptake, glutamate decarboxylase or choline acetyltransferase, in the pontine nuclei

https://doi.org/10.1016/0306-4522(83)90191-4Get rights and content

Abstract

The corticopontine fibres were severed in the crus cerebri in rats and mice by a stereotaxically operated retractable wire-knife. The pontine nuclei were microscopically dissected from fresh slices of rats and synaptosome-containing homogenates were prepared. The high affinity uptake of radiolabelled l-glutamate (l-Glu) and d-aspartate (d-Asp) was heavily reduced five days after the lesions. The uptake was further reduced after bilateral (−75% for d-Asp and −65% for l-Glu) than after unilateral lesions (−55% for d-Asp and −45% to −50% for l-Glu on the lesioned side). The molar ratio of the uptakes of d-Asp and l-Glu was consistently lower in pons after transection of the cortical afferents than normally (− 28% after bilateral lesions). γ-Aminobutyrate uptake and glutamic acid decarboxylase were not changed. Choline acetyltransferase was increased (+ 53%) after unilateral lesions, but not altered after bilateral lesions. Autoradiograms of slices from mice, incubated with tritium-labelled amino acids and fixed in glutaraldehyde, showed high affinity uptake sites for d-Asp to be enriched in the pontine nuclei, compared to neighbouring structures. After partial lesion of the crus cerebri the uptake was reduced in the area with degenerated corticopontine afferents. γ-Aminobutyrate uptake sites were relatively less concentrated in the pontine nuclei than d-Asp uptake sites.

The results indicate, along with the previous demonstration of Ca-dependent K-induced release of d-[3H]aspartate from the corticopontine terminals,41 that glutamate and/or aspartate may be transmitters in this pathway. The results also suggest that acidic amino acid uptake sites may differ in their relative transport rates for aspartate and glutamate.

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    *

    W. T. was on leave of absence from the Faculty of Science, Mahidol University, Rama VI Road, Bangkok 4, Thailand. Present address: MRC Developmental Neurobiology Unit, Institute of Neurology, 33 John's Mews, London WC1N 2NS, England.

    Institute of Physiology, University of Oslo, Oslo 1, Norway.

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