G R González Burgos

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The effect of gamma-aminobutyric acid (GABA) on synaptic transmission in rat superior cervical ganglion (SCG) was assessed in vitro by extracellular recording. Postganglionic compound action potentials (CAPs) triggered by preganglionic stimulation were blocked in a reversible and concentration-dependent fashion by short, 60 s long, superfusion with GABA(More)
We have compared the effect of calcium channel blockers on the potassium-evoked release of tritium-labeled acetylcholine and on preganglionic spike-evoked synaptic transmission in the rat superior cervical ganglion. Transmitter release at the nerve terminals is mediated by the influx of calcium through voltage-gated calcium channels. While four types of(More)
This study aimed at examining the effect of thyroid hormones on cholinergic transmission in isolated rat superior cervical ganglia (SCG). In SCG explants incubated with 3H-choline, thyroxine (T4) and 3,3',5-triiodothyronine (T3) added to the medium before a second depolarization stimulus of 60 mM K+ resulted in a dose-dependent increase of S2/S1 ratio for(More)
Activity-dependent changes of synaptic efficacy in the superior cervical ganglion (SCG) can be prevented by gamma-aminobutyric acid (GABA). We have studied the effects of picrotoxin (PTX) on GABA-mediated inhibition of long-term potentiation (LTP) of synaptic transmission in the rat SCG. Compound action potentials were recorded extracellularly in the(More)
The in vitro capacity of sympathetic superior cervical ganglia (SCG) to take up [3H]choline from the extracellular medium, to synthesize acetylcholine from [3H]choline, and to release [3H]acetylcholine in response to a high K+ concentration, were examined in rats throughout a 24-h cycle. Both the release of [3H]acetylcholine and the synthesis of(More)
Some characteristics of gamma aminobutyric acid (GABA) uptake and release in rat superior cervical ganglion (SCG) were investigated. Kinetic analysis of GABA uptake indicated the existence of both high affinity (Km = 18.6 microM) and low affinity (Km = 485 microM) uptake systems. 3H-GABA influx was decreased by inhibitors of glial (beta-alanine), neuronal(More)
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