PubMed · 2297097
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D J Cole, M W Kalichman, H M Shapiro, E I Eger. 1990. Does 1 + 1 = 2? A continuing debate.. https://doi.org/10.1213/00000539-199001000-00038
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To determine the relationship between cerebral Glc metabolism and glutamatergic neuronal function, we used 13C NMR spectroscopy to measure, simultaneously, the rates of the tricarboxylic acid cycle and Gln synthesis in the rat cortex in vivo. From these measurements, we calculated the rates of oxidative Glc metabolism and glutamate-neurotransmitter cycling between neurons and astrocytes (a quantitative measure of glutamatergic neuronal activity). By measuring the rates of the tricarboxylic acid cycle and Gln synthesis over a range of synaptic activity, we have determined the stoichiometry between oxidative Glc metabolism and glutamate-neurotransmitter cycling in the cortex to be close to 1:1. This finding indicates that the majority of cortical energy production supports functional (synaptic) glutamatergic neuronal activity. Another implication of this result is that brain activation studies, which map cortical oxidative Glc metabolism, provide a quantitative measure of synaptic glutamate release.
The neuroactive steroid 5 beta-pregnan-3 alpha-ol-20-one (5 beta 3 alpha) modulates GABAA receptor function by potentiating postsynaptic GABA currents. While much is now known about the postsynaptic action of neurosteroids, far less is known about how they affect neurotransmission. We have investigated the synaptic actions of 5 beta 3 alpha in a simple vertebrate model, the embryo of the clawed toad, Xenopus laevis, in which a known GABAergic pathway, activated by the rostral cement gland, terminates swimming when the animal contacts an obstruction. Cement gland stimulation evokes bicuculline-sensitive inhibitory postsynaptic potentials (IPSPs) in motorneurones that terminate swimming and which are greatly enhanced by the presence of (1-5 microM) 5 beta 3 alpha. In the presence of TTX, depolarising inhibitory potentials are recorded with KCl-filled microelectrodes reflecting the spontaneous release of transmitter. The majority are glycinergic with durations of 20-80 ms and are blocked by strychnine while the remainder are GABAergic with durations of 90-200 ms and are abolished by bicuculline. We show here that, in the presence of 5 beta 3 alpha, the spontaneous GABA IPSPs lengthen dramatically in some cases to over 500 ms, but the glycine potentials are unaffected. The steroid has no other detectable postsynaptic effects in that the range of amplitudes of GABA potentials is unaffected and there is no change in the resting membrane potential. However, 5 beta 3 alpha also caused a marked increase in the rate of occurrence of spontaneous GABA potentials. This suggests a novel presynaptic site of action in which the steroid enhances the probability of vesicular GABA release from GABA terminals.
A high-performance liquid chromatographic (HPLC) method for the determination of oxolinic acid (OA) in the plasma of seabass (Dicentrarchus labrax) anaesthetized with 2-phenoxyethanol is described. The samples were extracted and cleaned up by a solid-phase extraction procedure using C18 extraction cartridges. After the eluent was evaporated, the dry residue was dissolved in 1/15 M phosphate buffer. OA was determined by using an isocratic HPLC method with UV detection at 340 nm. Seabass drug-free plasma samples were spiked with OA at 0.2, 1.0, 5.0 and 25.0 microg/ml. Validation of the method showed good precision and accuracy. The mean recovery was 92.2%, with a relative standard deviation lower than 5%. The quantification limit was 0.2 microg/ml. The method was tested on 300 plasma samples of OA-treated seabass.