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 3H release. The concentration of hormone that produced 50% of maximal increase in K+-induced radioactivity release was 8 × 10–9 M for T4 and 1.6 × 10–8M for T3 while 3,3’,5,5’-tetraiodothyroacetic acid was almost ineffective. Preincubation of SCG with 10–7M iopanoic acid for 30 min before S2, although not affecting by itself S2/S1 ratio, effectively prevented the increase given by T4 or T3. 3H-acetylcholine release by SCG was augmented in a high K+ and the effect was amplified by T4 to a similar extent as that for total 3H release. When added to the incubation medium together with 60 mM K+ for 30 min, T4 (10–7M) increased significantly the activity of choline acetyltransferase (ChAT). T4 did not affect ChAT activity in SCG exposed to 4.7 mM K+, nor in SCG homogenates. 3H-choline uptake measured immediately after exposure of SCG to 60 mM K+ decreased by 25%, whereas it increased by 71% after a subsequent 30-min incubation with 4.7 mM K+. Addition of 10–7M T4 prevented the changes in choline uptake observed in a high K+ medium. These results indicate that T4 increases SCG cholinergic transmission.
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 (2,4-diaminobutyric acid, DABA), or glial and neuronal GABA uptake (nipecotic acid). 3H-GABA efflux was elicited by K+ depolarization in a dose-dependent manner, an effect unaltered by severing the preganglionic nerve fibers. Superfusion of SCG explants with DABA or beta-alanine resulted in increased 3H-GABA efflux from tissue, an effect amplified by the absence of calcium in the superfusion medium. 3H-GABA loading in the presence of DABA, but not in the presence of beta-alanine, resulted in abolition of K(+)-elicited 3H release. At 20 mM, but not at 50 mM K+, the release of 3H-GABA was inhibited by replacing Ca2+ by Mg2+ and by adding EGTA, or by incubating SCG in the presence of the Ca(2+)-channel blocker verapamil. Veratrine evoked GABA release in Ca(2+)-independent manner. None of several putative SCG autacoids or agonists (nicotine, muscarine, norepinephrine, dopamine, serotonin, baclofen, muscimol) significantly modified GABA release.
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