Neurotransmission and glial cells: a functional relationship?
The investigations reported here demonstrate high affinity transport systems localized in glial cells which appear to be specific for amino acid neurotransmitter candidates. Data on uptake of gamma-aminobutyric acid (GABA), glutamate, glycine, and taurine, show transport systems with KT'S in the range of 10(-5) M. In addition, the distribution of the glial transport system for glycine is shown to parallel the presumed distribution of glycine as an inhibitory neurotransmitter. Results of these studies also suggest that transport studies on brain homogenates or synaptosomal preparations do not serve to localize these functions to synaptic elements as is widely believed. This report shows that glia can form vesicles during homogenization which band which synaptosomes in density gradients, and retain transport activity. Glia also may contribute to the release of neurotransmitters via control of the extracellular Ca++ concentration. This is shown by the ability of GABA in the extracellular media to cause release of Ca++ by glia.
Neurotransmission and glial cells: a functional relationship? The investigations reported here demonstrate high affinity transport systems localized in glial cells which appear to be specific for amino acid neurotransmitter candidates. Data on uptake of gamma-aminobutyric acid (GABA), glutamate, glycine, and taurine, show transport systems with KT'S in the range of 10(-5) M. In addition, the distribution of the glial transport system for glycine is shown to parallel the presumed distribution of glycine as an inhibitory neurotransmitter. Results of these studies also suggest that transport studies on brain homogenates or synaptosomal preparations do not serve to localize these functions to synaptic elements as is widely believed. This report shows that glia can form vesicles during homogenization which band which synaptosomes in density gradients, and retain transport activity. Glia also may contribute to the release of neurotransmitters via control of the extracellular Ca++ concentration. This is shown by the ability of GABA in the extracellular media to cause release of Ca++ by glia.