TY - JOUR
T1 - Calcitonin and calcitonin gene-related peptide enhance calcium-dependent potentials
AU - Nohmi, Mitsuo
AU - Shinnick-Gallagher, Patricia
AU - Gean, Po Wu
AU - Gallagher, Joel P.
AU - Cooper, Cary W.
N1 - Funding Information:
We thank Drs. M. Thomas, B. Williams and K. Hi-rai for their careful reviews of the manuscript. Supported by NS16228 to P.S.G.
PY - 1986/3/5
Y1 - 1986/3/5
N2 - Recent data suggests that calcitonin (CT) and/or calcitonin gene-related peptide (CGRP) may be potential transmitters or modulators in the nervous system. The present study analyzed the effect of CT and CGRP on the neuronal membranes of cat parasympathetic ganglia of the urinary bladder. The related peptides prolonged the duration of the afterhyperpolarization of the action potential but had no effect on resting potential or input resistance. CT and CGRP enhanced the duration of a calcium spike recorded in the presence of agents blocking Na and K channels while under similar conditions forskolin, an activator of adenylate cyclase, did not affect the calcium spike. These data suggest that the neural mechanism of action of CT and CGRP is to prolong a calcium conductance and that these effects are not mediated through cyclic AMP.
AB - Recent data suggests that calcitonin (CT) and/or calcitonin gene-related peptide (CGRP) may be potential transmitters or modulators in the nervous system. The present study analyzed the effect of CT and CGRP on the neuronal membranes of cat parasympathetic ganglia of the urinary bladder. The related peptides prolonged the duration of the afterhyperpolarization of the action potential but had no effect on resting potential or input resistance. CT and CGRP enhanced the duration of a calcium spike recorded in the presence of agents blocking Na and K channels while under similar conditions forskolin, an activator of adenylate cyclase, did not affect the calcium spike. These data suggest that the neural mechanism of action of CT and CGRP is to prolong a calcium conductance and that these effects are not mediated through cyclic AMP.
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U2 - 10.1016/0006-8993(86)91616-1
DO - 10.1016/0006-8993(86)91616-1
M3 - Article
C2 - 2421835
AN - SCOPUS:0022548239
SN - 0006-8993
VL - 367
SP - 346
EP - 350
JO - Brain Research
JF - Brain Research
IS - 1-2
ER -