Effect of parathyroid hormone and calcitonin on acetylcholine release in rat sympathetic superior cervical ganglion

Javier E. Stern, Daniel P. Cardinali

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3 Scopus citations


The effects of parathyroid hormone (PTH) and calcitonin on acetylcholine release by rat superior cervical ganglion (SCG) were evaluated in vitro. SCG labeled with [3H]choline were exposed to four 5 min-long pulses of 40 mM K+, 35 min apart. PTH increased, and calcitonin inhibited, in a dose-dependent way, K+-elicited [3H]acetylcholine release, with apparent effective doses 50 of about 10-9 M. The effect of PTH was inhibited by co-incubation with the PTH receptor antagonist NLe [8-18]-PTH (3-34) amide. Incubation of SCG for 120 min with PTH or calcitonin resulted in dose-dependent augmentation or inhibition of K+-induced increase of high affinity [3H]choline uptake, respectively, with a maximal effect at 10-8 M concentration (PTH) and 10-9 M concentration (calcitonin) and declining at higher concentrations. The increase in SCG [3H]choline uptake induced by PTH was blunted by preincubation with the PTH antagonist NLe [8-18]-PTH (3-34) amide. At 10-7 M concentrations, PTH increased significantly the in vitro conversion of [3H]choline to [3H]acetylcholine, an effect inhibited by PTH receptor antagonist. Calcitonin did not modify SCG [3H]acetylcholine synthesis by rat SCG. The results indicate that, in vitro, PTH increases, and calcitonin inhibits, acetylcholine release in rat SCG.

Original languageEnglish (US)
Pages (from-to)267-274
Number of pages8
JournalBrain Research
Issue number2
Publication statusPublished - Jul 11 1994



  • Acetylcholine
  • Calcitonin
  • Choline acetyltransferase
  • Parathyroid hormone
  • Superior cervical ganglion
  • Transmitter release

ASJC Scopus subject areas

  • Neuroscience(all)
  • Molecular Biology
  • Clinical Neurology
  • Developmental Biology

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