TY - JOUR
T1 - Effect of parathyroid hormone and calcitonin on acetylcholine release in rat sympathetic superior cervical ganglion
AU - Stern, Javier E.
AU - Cardinali, Daniel P.
N1 - Funding Information:
These studies were supported by grants from the University of Buenos Aires and the Consejo Nacional de Investigaciones Cientificas y Tdcnicas, Argentina. The technical advice of Lic. Guillermo Gonzfilez Bur-gos in the initial phase of the study is gratefully acknowledged.
PY - 1994/7/11
Y1 - 1994/7/11
N2 - 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.
AB - 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.
KW - Acetylcholine
KW - Calcitonin
KW - Choline acetyltransferase
KW - Parathyroid hormone
KW - Superior cervical ganglion
KW - Transmitter release
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U2 - 10.1016/0006-8993(94)91791-4
DO - 10.1016/0006-8993(94)91791-4
M3 - Article
C2 - 7953692
AN - SCOPUS:0028307137
VL - 650
SP - 267
EP - 274
JO - Brain Research
JF - Brain Research
SN - 0006-8993
IS - 2
ER -