Glutamate in some retinal neurons is derived solely from glia

Adenosine receptors were made visible on light microscopy by autoradiography with tritiated cyclohexyladenosine. In the cerebellum, adenosine receptors were absent in Weaver mice, which lack granule cells, and were displaced in Reeler mice, which have displacements of granule cells. Thus, adenosine receptors appear to be located on the axon terminals of excitatory granule cells in the cerebellum. Removal of one eye of a rat depleted adenosine receptors in the contralateral superior colliculus, suggesting that the receptors occur on axon terminals of excitatory projections from retinal ganglion cells. The presence of adenosine receptors on excitatory axon terminals may explain synaptic inhibition by adenosine and the behavioral effects of xanthines.

https://science.sciencemag.org/content/sci/220/4600/967.full.pdf

Adenosine receptors: autoradiographic evidence for their location on axon terminals of excitatory neurons

Functions of ionotropic and metabotropic glutamate receptors in sensory transmission in the mammalian thalamus

The distribution of the neuroactive amino acids glutamate, GABA, and glycine in the human retina was examined in consecutive semithin sections treated with antisera specific for fixed glutamate, GABA, and glycine, respectively.



Glutamate immunoreactivity was conspicuous in all photoreceptor cells (rods more strongly labelled than cones), and in a majority (85–89%) of the cells in the inner nuclear layer (INL). Rod spherules and cone pedicles showed a greater enrichment of glutamate immunoreactivity than the parent cell bodies and inner segments. Also, structures of the inner plexiform layer (IPL) were labelled. A large majority (83–91%) of cells in the ganglion cell layer (GCL) was strongly stained, as were most axons in the nerve fibre layer. Muller cell processes appeared unstained.



GABA immunoreactivity was present in presumed amacrine but not in bipolar-like cells. The stained cells were restricted to the inner ⅓ of the INL and were more frequent in central than in peripheral retina (40% and 26% of all cells in the inner ⅓of INL, respectively). GABA positive cell processes, probably originating from interplexiform cells, appeared to traverse the INL and end in the outer plexiform layer. Dense immunolabeling was found in the IPL. GABA immunoreactive cells (some also stained for glutamate) comprised 23% of all GCL cells in the peripheral retina, but only 5% in the central retina. Most of them were localized adjacent to the IPL. A few GABA positive (possibly ganglion) cells extended a single fibre toward the nerve fibre layer. Solitary GABA positive fibres were seen in this layer and in the optic nerve.



Glycine immunoreactivity was observed in cells with the location typical of amacrine and bipolar (peripheral retina) cells, as well as in punctate structures of the IPL. In contrast to the GABA positive cells, the glycine positive cells were more frequent in the peripheral than in the central retina (42% and 23% of all cells in inner ⅓ of INL, respectively). A few cells in the GCL (0.5–1.5%) were glycine positive.



Glutamate colocalized with GABA or glycine in a majority of the cells stained for either of these inhibitory transmitters (90–95% of the GABA positive cells, and 80–86% of the glycine positive cells, in the INL). Some bipolar cells were stained for both glutamate and glycine. Colocalization of GABA and glycine occurred in a subpopulation (3–4%) of presumed amacrine cells, about half of which was also glutamate positive.

Glutamate, GABA, and glycine in the human retina: an immunocytochemical investigation.

Aspartate-like and glutamate-like immunoreactivities in the inferior olive and climbing fibre system: a light microscopic and semiquantitative electron microscopic study in rat and baboon (Papio anubis).

Glutamate (Glu) and aspartate (Asp) are considered to be major excitatory neurotransmitters in the central nervous system1, but since the Jasper and Koyama report2, the release of endogenous Glu or Asp on stimulation of an appropriate pathway in vivo has received little attention. They have been proposed as transmitters in the optic nerve of the pigeon (Columbalivia)3–7. We now report that, using a push–pull cannula technique, the concentrations of Glu, Asp, glycine (Gly) and γ-aminobutyric acid (GABA) have been determined by mass fragmentography in perfusates from the optic tectum on electrical stimulation of the optic nerve or of the midbrain nucleus isthmi, pars parvocellularis (Ipc). Optic nerve stimulation markedly increased the content of Glu and Asp in the perfusate whereas stimulation of the nucleus Ipc was ineffective. The amount of GABA collected was increased only during Ipc stimulation. We conclude that Glu, Asp or related substances are involved in the transmission of the pigeon optic nerve terminals.

In vivo release of glutamate and aspartate following optic nerve stimulation

Gas chromatographic method for the determination of trace amounts of putative amino acid neurotransmitters from brain perfusates collected in vivo.

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In vivo release of glutamate and aspartate following optic nerve stimulation

Gas chromatographic method for the determination of trace amounts of putative amino acid neurotransmitters from brain perfusates collected in vivo.