Fifty Years of Biochemistry. A Personal Account

Quastel, J. H.

doi:10.1139/o74-012

Cited by 9 publications

(2 citation statements)

References 15 publications

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“…A reduction in neurotransmission efficacy might arise from a rerouting of the neurotransmitters for metabolic purposes as has been proposed to account for impaired neurotransmission in the brain during hypoglycaemia (Quastel, 1974). In support of this idea, the overall metabolic status of brain slices remained stable during hypoglycaemia while synaptic transmission was disrupted (Lewis et al.…”

Section: Glutamate Catabolism and Retinal Functionmentioning

confidence: 99%

“…As glutamate is the major retinal excitatory neurotransmitter, one possibility is that the b‐wave loss reflects altered neurotransmission between photoreceptors and ON‐bipolar cells (Slaughter & Miller, 1981; Stockton & Slaughter, 1989; Robson & Frishman, 1995). Reduced neurotransmission might occur secondary to increased glutamate oxidation to provide metabolic substrates (Quastel, 1974); thus cellular localization would allow the identification of specific metabolic pathways within neuronal or glial cells. We have previously demonstrated that, secondary to 4‐CIN application, inhibiting glutamate‐utilizing enzymes suppressed the b‐wave recovery induced by exogenous substrates (Bui et al.…”

Section: Introductionmentioning

confidence: 99%

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Monocarboxylate transport inhibition alters retinal function and cellular amino acid levels

Bui

Wellard

Kalloniatis

2004

Eur J of Neuroscience

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We assessed the effect of the in vivo application of monocarboxylate transport inhibitors on retinal function and amino acid immunocytochemistry. We wanted to determine the impact that altered aerobic metabolite availability has on retinal function and the characteristics of amino acid shunting into metabolic pools. Electroretinograms were collected from anaesthetized rats at various times after intravitreal injection of the monocarboxylate transport inhibitors alpha-cyano-4-hydroxycinnamate (4-CIN; 2 micro L, 0.1-10 mm) or p-(dipropylsulphamoyl)benzoic acid (probenecid; 1-10 mm). Changes in retinal function were compared with quantitative amino acid immunocytochemical changes in retinas harvested 20 and 40 min after either 4-CIN or vehicle treatment. The injection of 4-CIN resulted in a dose-dependent reduction of the ON-bipolar cell P2 wave amplitude (20-80%) and delay in its implicit time. The phototransduction sensitivity was mildly reduced whereas the ON-bipolar cell P2 sensitivity was unaffected. Probenecid induced functional changes similar to those observed with 4-CIN. We also mapped the amino acid alterations within specific cell classes induced by 4-CIN application. All neurones displayed a reduced glutamate content averaging 48%; reduced GABA (31%) and glycine (28%) were found within amacrine cells and glutamine was reduced in all cell classes except photoreceptor and Müller cells. All cell classes in the retina demonstrated increases in aspartate (57%), whereas leucine (24%) and ornithine (21%) were only significantly increased in photoreceptor and bipolar cells. The reduction in glutamate immunolabelling in specific retinal cell classes was mirrored by an increase in aspartate levels at these locations. In addition, attenuated glutamine immunolabelling also closely matched the spatial pattern observed for glutamate. Our immunocytochemical analysis provides evidence that monocarboxylate transport inhibition induces a shift in the equilibrium of glutamate transamination reactions involving aspartate throughout the retina whereas photoreceptor and bipolar cells also use glutamate transamination reactions involving ornithine and leucine. The distribution pattern of glutamine secondary to monocarboxylate inhibition suggests that this amino acid is a major precursor for glutamate throughout the retina.

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Section: Glutamate Catabolism and Retinal Functionmentioning

confidence: 99%